Handbook of Child and Adolescent Anxiety Disorders

Dean McKay
Eric A. Storch Editors
Handbook
of Child and
Adolescent
Anxiety Disorders
Second Edition
Handbook of Child and Adolescent
Anxiety Disorders
Dean McKay • Eric A. Storch
Editors
Handbook of Child
and Adolescent Anxiety
Disorders
Second Edition
Editors
Dean McKay Eric A. Storch
Department of Psychology Department of Psychiatry
Fordham University and Behavioral Sciences
Bronx, NY, USA Baylor College of Medicine
Houston, TX, USA
ISBN 978-3-031-14079-2 ISBN 978-3-031-14080-8 (eBook)

https://doi.org/10.1007/978-3-031-14080-8
© The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature
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Contents
Part I
1
Classification of Child and Adolescent Anxiety Disorders �� 3
Dean McKay and Eric A. Storch
2 Issues in Differential Diagnosis: Phobias
and Phobic Conditions�� 7
Mark B. Powers, Kiara Leonard, Maris Adams, Emma Turner,
Jamie R. Pogue, Marjorie L. Crozier, Emily Carl,
and Seth J. Gillihan
3 Issues in Differential Diagnosis: Considering Generalized
Anxiety Disorder, Obsessive-Compulsive Disorder,
and Posttraumatic Stress Disorder�� 29
Nicole Fleischer, Jonathan Rabner, Julia Spandorfer,
and Philip C. Kendall
4 Cognitive Behavioral Models of Phobias
and Pervasive Anxiety�� 45
Dean McKay
5
Neurochemistry of Childhood Anxiety Disorders �� 55
Lauren Havel, Pranav Mehta, Ankit Gautam,
Edward Danielyan, and Kirti Saxena
6
Genetics of Childhood and Adolescent Anxiety
and Obsessive-Compulsive Disorders�� 73
Paul D. Arnold, Lilit Antonyan, Francis Routledge,
and Sandra Meier
7 Taxometric Methods in Child and Adolescent
Anxiety Disorders�� 97
Christian A. Hall and Joshua J. Broman-Fulks
8
Dimensional Diagnosis of Anxiety in Youth �� 111
Dean McKay
9 Transdiagnostic Treatment Models for Child
and Adolescent Anxiety Disorders�� 125
Ashley R. Karlovich, Elizabeth R. Halliday,
and Jill Ehrenreich-May
v
vi Contents
Part II
10 Differential
Diagnosis of Attention Deficit Hyperactivity
Disorder (ADHD) in Child and Adolescent Anxiety �� 141
Alasdair Vance, Jo Winther, and Elham Shoorcheh
11 Comorbid
and Secondary Depression in Child
and Adolescent Anxiety�� 157
Robert W. Garvey, Michelle K. Hiner, Chris A. Kelly,
and Margaret S. Andover
12 The
Role of Disgust in Childhood Anxiety Disorders �� 173
Ana Rabasco and Dean McKay
13 Problems
in Emotion Regulation in Child and Adolescent
Anxiety Disorders Section: Diagnostic Components
of Child and Adolescent Anxiety Disorders �� 191
Kristel Thomassin, Marni L. Jacob, Kara B. West,
Molly E. Hale, and Cynthia Suveg
14 Emergent
Personality Features in Adolescent
Amanda Venta and Jaime L. Anderson
15 Family
Components of Child and Adolescent
Amanda Palo and Abigail Candelari
Part III
16 Specific
Phobias in Children and Adolescents�� 235
Thompson E. Davis III, Jerrica Guidry,
and Thomas H. Ollendick
17 Separation
Anxiety Disorder in Children and Adolescents�� 249
Nicole E. Caporino, Joyce X. Wong,
and Arianna O’Brien Cannon
18 The
Treatment of Generalized Anxiety Disorder in Youth�� 271
Carl F. Weems and R. Enrique Varela
19 Selective Mutism�� 287
Karin L. Price, Natalie Delgado, and Kelly N. Banneyer
20 Treatment
of Social Anxiety in Children and Adolescents �� 299
Tracy L. Morris and Johann D’Souza
21 Treatment
of Pediatric Post-traumatic Stress Disorder �� 315
Elissa J. Brown, Komal Sharma-Patel, Kaitlin Happer,
and Amy Hyoeun Lee
Contents vii
22 Obsessive-Compulsive Disorder in Children

and Adolescents�� 331
Allie N. Townsend, Johann M. D’Souza, Andrew G. Guzick,
and Eric A. Storch
23 Pharmacological Treatment of Anxiety Disorders
in Children and Adolescents �� 347
Sohail Nibras, Anh Truong, and Laurel L. Williams
24 Common Mechanism for Anxiety Disorders
A
and Drug Addiction: Implications for Current
and Novel Pharmacological Treatments�� 357
Marco A. Grados and Bushra Rizwan
Part IV
25 Food Neophobia in Children: Misnomer, Anxious Arousal,

or Other Emotional Avoidance? �� 367
Dean McKay and Charlene Minaya
26
Anxiety-Related Problems in Developmental Disabilities�� 379
Morgan M. McNeel, Emily R. Jellinek, and Eric A. Storch
27 Treatment of Youth Anxiety in the Context of Family
Dysfunction and Accommodation�� 395
Rebecca G. Etkin and Eli R. Lebowitz
28 Parent Training for Childhood Anxiety �� 411
Adam B. Lewin and Kelly Kudryk
29 School-Based Interventions for Child
and Adolescent Anxiety�� 425
Jeremy K. Fox, Samantha Coyle, Taylor Walls, Avi Kalver,
Marcus Flax, Aleta Angelosante, and Carrie Masia Warner
30
Social Disability and Impairment in Childhood Anxiety �� 445
Laura John-Mora, Abigail M. Ross, and Jordana Muroff
Index�� 469
Part I
Classification of Child
and Adolescent Anxiety Disorders 1
Dean McKay and Eric A. Storch
Classification in psychopathology has moved classify newly discovered entities. Again, contro-
through several important stages, based on the tra- versies exist (e.g., cloud theory versus heliocen-
jectory of the Diagnostic and Statistical Manual tric theory of atomic structure; Cox, 1996), but
from its first edition to the current, fifth edition. these do not substantially alter the manner of uti-
The initial two editions were marked by a unify- lizing the classification system.
ing theoretical basis whereby specific diagnoses Unlike other branches of science, however,
were conceptualized in psychodynamic terms. psychiatry, psychology, and their associated pro-
This tradition is similar to the formulation of tax- fessions are not unified by a single theory of mind,
onomies in other branches of science. For exam- and most conditions likely have multiple determi-
ple, in biology the reliance on a hierarchical nants. Further, most users of the original DSMs
arrangement from kingdom down to species is noted the limited reliability of the taxonomy it laid
based on a specific theoretical framework whereby out, and with the third edition came a radical
all newly discovered organisms may be readily change in how psychiatric classification was con-
classified. While not totally without controversy, ceptualized: purely descriptive and atheoretical.
such as the movement toward cladistics (whereby This allowed users to arrive at diagnoses with
organisms are classified by ancestry rather than much greater precision, and the aim was to estab-
present biological structure; Scott-Ram, 2008; lish a set of conditions that had ecological and syn-
Williams & Ebach, 2020), these represent mere dromal validity. This has served the field well and
refinements rather than sea-change level altera- has led to important advances in assessment, treat-
tions in classification. Another example is in ment, and etiological understanding. However,
chemistry, where elements are classified by a the- unlike classification systems in other branches of
ory-driven framework regarding the organization science, should a new condition arise, there is no
of atoms, with specifications within the periodic inherent mechanism for classifying it. Instead, any
table of elements (such as noble gases, metals, new diagnosis must wait until the revisions are
etc.) that also readily guides researchers in how to planned for the next edition of the DSM, where-
upon the proposed diagnosis is determined by
D. McKay (*) committee. The current edition (the DSM-5-TR;
Department of Psychology, Fordham University,
American Psychiatric Association, 2022) lays out
Bronx, NY, USA
e-mail: mckay@fordham.edu diagnoses in a single-axial framework that remains
committee-driven. The recent text revision aims to
E. A. Storch
Department of Psychiatry and Behavioral Sciences, address racial and cultural disparities present in
Baylor College of Medicine, Houston, TX, USA prior editions (Canady, 2022).
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 3

D. McKay, E. A. Storch (eds.), Handbook of Child and Adolescent Anxiety Disorders,
https://doi.org/10.1007/978-3-031-14080-8_1
4 D. McKay and E. A. Storch
This process of committee-driven descriptive LeDoux, 2009; LeDoux & Schiller, 2009; Marek
diagnoses has led to a growth of diagnoses, but & Sah, 2018). This leaves us with the curious
rarely have any been eliminated. In the anxiety problem of a biologically based theoretical
disorders, two disorders stand out as illustrative framework from which many disorders will be
of this point. On the one hand, agoraphobia with- classified but that also fails to adequately explain
out history of panic has been in the DSM since a serious and debilitating condition that is con-
the arrival of the third edition. However, this par- sidered a putative member. Moreover, although
ticular diagnosis has long been recognized as other etiological features are considered in this
either so rare as to not exist, or when actually framework, there is the distinct possibility of an
diagnosed to likely have had a panic-related ori- inaccurate bias towards a neurobiological expla-
gin even if panic is completely and successfully nation for disorders against a more holistic under-
avoided by the sufferer (McNally, 1994). On the standing that incorporates multiple
other hand, of the very few diagnoses that have determinants.
been eliminated is overanxious disorder of child-
hood. Interestingly, this diagnosis was only elim-
inated in that the criteria for a different disorder urrent Standing of Childhood
C
(generalized anxiety disorder) were extended to Anxiety Diagnosis
encompass diagnosis in children. While these are
but two examples, they typify the approach to the At the present time, most of the anxiety disorders
DSM as contemporarily construed. Committees in the DSM are age-downward extensions of
determine putative diagnoses for larger catego- adult diagnoses. The exceptions to this are sepa-
ries, based on the existing literature on etiology, ration anxiety, school refusal, and selective mut-
incidence, and prevalence. At the same time, ism. While there are exceptions, all anxiety
existing diagnoses are very rarely eliminated, disorders, when present in children, have unique
even if infrequently encountered or its basis is manifestations that call for special clinical skill
seriously questioned by the broader community in assessment and intervention. One important
of researchers for that disorders’ member class. distinction between childhood and adult manifes-
The advent of the DSM-5 has included several tations of anxiety is that it is not required or even
new diagnoses and categories. For example, there expected that children have clear insight into the
is now the obsessive-compulsive related disor- nature of their fears. The only adult disorder
ders, which includes the new diagnoses of hoard- where insight is not required is OCD (now part of
ing disorder (a condition rarely present in a separate class of disorders, but still marked by
children), and excoriation disorder. No anxiety extreme anxiety), and in this case, the modifier
disorders were eliminated in the most recent “with poor insight” or “with mixed insight” is
version. available in the DSM-5-TR, and this manifesta-
When the first edition of this book was being tion has come under specific scrutiny as a poor
prepared, the DSM-5 was in the later stages of prognostic indicator for treatment response (i.e.,
development. At the time, many of the proposed McKay et al., 2010).
changes for the fifth edition of the DSM included A second major distinction involves the
the potential role of fear circuitry modeling for behavioral manifestation of different anxiety dis-
conceptualizing candidate disorders (i.e., Britton orders. In children, it is not unusual for the pre-
& Rauch, 2009). This did not fully manifest in sentation to have clear developmental
the final version of the manual. Additionally, the consequences. For example, children with school
various proposed neural circuitry models did not refusal, when untreated, face significant develop-
readily account for learning processes that might mental limitations resulting from reduced social-
influence changes in the connectivity among ization and limited opportunities for establishing
putative brain areas, despite repeated findings normative age-related behaviors. This is likewise
from neuroscientists to the contrary (Debiec & true in social anxiety and the dimensionally less
1 Classification of Child and Adolescent Anxiety Disorders 5
severe problem of chronic shyness, whereby the such as behavioral and cognitive theory (Taylor
inhibition associated with the disorder leads to et al., 2009).
developmental lags (Beidel & Turner, 2006; This leaves the field in a difficult predicament.
Ranta et al., 2015). Given the importance of It appears that, in consolidating a research agenda
socialization to cognitive and emotional growth that would advance our approach to classifica-
(Konner, 2010), when treating children with anx- tion, it will be necessary to identify the variables
iety disorders, it is often also necessary to attend associated with the greatest amount of variance
to socialization problems resulting from the in the developmental trajectory of anxiety per se
avoidance behaviors involved. and all its manifestations. This would no doubt
A third major distinction involves the role of narrow the class of disorders, but would also
caregivers in the etiology and maintenance of allow for a comprehensive theory for which clas-
anxiety. While this is in part associated with sification would readily flow without simply
socialization (i.e., Lawrence et al., 2019; Okagaki adhering to a diagnosis by committee approach
& Luster, 2005), it is unique in that each is mutu- to classification. It would also require that
ally dependent. This unique association can lead researchers remain open to a wide range of dispa-
to anxiety problems in children if one or both rate theoretical influences (i.e., biological, psy-
caregivers are themselves anxious, or if they chological, developmental) to converge into a
engage in behaviors designed to accommodate single meaningful theoretical framework.
anxious avoidance (see Chap. 20, this volume). Since the state of the field is not integrated
This is distinct from mere genetic transmission, into a meaningful theoretical framework, there
since there are specific behaviors parents may are numerous perspectives on conceptualization,
exhibit that propagate anxiety exclusive of herita- diagnosis, and treatment. It is our hope that the
bility by virtue of reducing the child’s anxiety. field will continue to advance whereby the mul-
Indeed, genetic data has been inconclusive with tiple perspectives in the field may be meaning-
respect to transmission of anxiety disorders, fully integrated to allow practitioners to
while behavioral theory has offered an empiri- seamlessly provide high quality services. In the
cally robust method of describing disorder onset meantime, this text is intended to provide a criti-
and maintenance (see Chap. 20, this volume). cal analysis of the state of the field in child and
Instead, it could be better stated that anxiety adolescent anxiety disorders across multiple per-
begets anxiety, but that there are no specific risks spectives. Since the publication of the first edi-
conferred on individual anxiety disorders. tion of this text, there has not, unfortunately, been
much progress on developing an integrated theo-
retical framework.
uture Directions in Classifying
F
Childhood Anxiety Disorders
Structure of the Present Text
The adequacy of a purely descriptive model of
psychopathology, with specific reference to anxi- We have arranged the book into four major sec-
ety disorders in childhood, is limited. Formerly, tions. The first is a foundational section related to
theoretically driven models seem inadequate diagnostic issues and the directions anticipated in
given the difficulties in operationalization and the coming years with respect to anxiety classifi-
reliability (such as that noted in the early editions cation in children. The second section examines
of the DSM). Modern medical conceptualiza- the full scope of alternative ways of classifying,
tions (such as the fear circuitry) do not yet have the adequacy of these approaches, and limita-
adequate empirical support to use in developing a tions, as well as complicating factors in anxiety
classification scheme. Further, purely biological disorder. The third section is devoted to specific
models are often viewed as overly reductionistic, childhood anxiety disorders and their treatment,
ignoring other important sources of influence as well as integrative approaches to therapy (such
6 D. McKay and E. A. Storch
as cognitive-behavioral therapy and psychophar- on the anxiety disorders: Implications for DSM-V and
beyond (pp. 107–126). Springer.
macology). Finally, the fourth section covers Konner, M. (2010). The evolution of childhood:
novel and emergent areas within the anxiety dis- Relationships, emotion, mind. Harvard University
orders in children. Press.
It is our hope that this book will serve the mul- Lawrence, P. J., Murayama, K., & Creswell, C. (2019).
Systematic review and meta-analysis: Anxiety and
tiple goals of providing clinicians with a deeper depressive disorders in offspring of parents with anxi-
understanding of the full breadth of childhood ety disorders. Journal of the American Academy of
anxiety disorders, their assessment, treatment, Child & Adolescent Psychiatry, 58, 46–60.
and a critical understanding of classification. We LeDoux, J. E., & Schiller, D. (2009). The human amyg-
dala: Insights from other animals. In P. J. Whelan &
also hope that this book will advance multiple E. A. Phelps (Eds.), The human amygdala (pp. 43–60).
research agendas such as those in specific anxiety Guilford.
disorders, as well as in areas that are debilitating Marek, R., & Sah, P. (2018). Neural circuits mediating
but have as yet received limited research scrutiny. fear learning and extinction. Systems Neuroscience,
21, 35–48.
Finally, and perhaps most importantly, we hope McKay, D., Taylor, S., & Abramowitz, J. S. (2010).
that this book will vastly improve the lives of Obsessive-compulsive disorder. In D. McKay, J. S.
children affected by anxiety disorders. Abramowitz, & S. Taylor (Eds.), Cognitive –behav-
ior therapy for refractory cases: Turning failure
into success (pp. 89–109). American Psychological
Association.
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Beidel, D. C., & Turner, S. M. (2006). Shy children, pho- (Eds.), Parenting: An ecological perspective (pp. 377–
bic adults: Nature and treatment of social anxiety dis- 410). Erlbaum.
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Britton, J. C., & Rauch, S. L. (2009). Neuroanatomy and Marttunen, M. (2015). Social anxiety and phobia in
neuroimaging of anxiety disorders. In M. M. Antony adolescents. Springer Nature.
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related disorders (pp. 97–110). Oxford University omy, and evolution. Cambridge University Press.
Press. Taylor, S., Asmundson, G. J. G., Abramowitz, J. S., &
Canady, V. A. (2022). DSM-5 text revision reflects updates McKay, D. (2009). Classification of anxiety disorders
in ethnic, racial issues. Mental Health Weekly, 32, 5–6. for DSM-V and ICD-11: Issues, proposals, and con-
Cox, P. A. (1996). Introduction to quantum theory and troversies. In D. McKay, J. S. Abramowitz, S. Taylor,
atomic structure. Oxford University Press. & G. J. G. Asmundson (Eds.), Current perspectives
Debiec, J., & LeDoux, J. E. (2009). The amygdala net- on the anxiety disorders: Implications for DSM-V and
works of fear: From animal models to human psycho- beyond (pp. 481–511). Springer.
pathology. In D. McKay, J. S. Abramowitz, S. Taylor, Williams, D. M., & Ebach, M. C. (2020). Cladistics: A
& G. J. G. Asmundson (Eds.), Current perspectives guide to biological classification. Cambridge Press.
Issues in Differential Diagnosis:
Phobias and Phobic Conditions 2
Mark B. Powers, Kiara Leonard, Maris Adams,
Emma Turner, Jamie R. Pogue, Marjorie L. Crozier,
Emily Carl, and Seth J. Gillihan
The purpose of this chapter is to summarize the objects or situations, specific phobias (formerly
current status of research with respect to the clin- “simple phobia” in DSM-III-R) can develop in
ical features, course, and prognosis of specific response to nearly anything (Marks, 1987).
phobias, social anxiety disorder (social phobia), Commonly occurring fears include animals,
panic disorder, agoraphobia, and separation anxi- heights, flying, enclosed spaces, darkness, receiv-
ety disorder in children. In this context, we will ing an injection, and seeing blood. Because chil-
consider the salient factors involved in the dif- dren naturally experience developmentally
ferential diagnosis of these five disorders. Finally, appropriate fears, it is important to distinguish
we will provide some directions to improve phobias from those fears that are typical for the
assessment of these disorders in children. developmental stage of the child and to recognize
their different forms of expression (e.g., tan-
trums, crying, freezing, clinging). A phobia diag-
Specific Phobia nosis should be considered when the fear is
excessive and causes marked interference in the
Description child’s life. In children, the fear must be present
for at least 6 months. According to DSM-5, spe-
Specific phobias are the most prevalent anxiety cific phobia should be diagnosed when all of the
disorder according to nearly all epidemiological following criteria are met (Table 2.1).
studies of the general population (e.g., Kessler These criteria for diagnosing specific phobias
et al., 2012). Defined in the Diagnostic and in children have been slightly modified from the
Statistical Manual of Mental Disorders Fifth criteria for the diagnosis in adults. The DSM-5
Edition (DSM-5; American Psychiatric categorizes specific phobias into five subtypes:
Association, 2013) as intense fears of specific animal phobias (e.g., spiders, dogs, snakes), nat-
ural environment phobias (e.g., storms, heights,
or water), blood-injection-injury phobias (e.g.,
M. B. Powers (*) · K. Leonard · M. Adams ·
seeing blood, receiving an injection/needles),
E. Turner · J. R. Pogue · E. Carl
Baylor University Medical Center, Dallas, TX, USA situational phobias (e.g., enclosed spaces, eleva-
e-mail: mark.powers1@bswhealth.org tors, flying), and other phobias for fears that do
M. L. Crozier not fit into one specific category (e.g., choking,
Brown University, Providence, RI, USA vomiting, loud sounds, costumed characters).
S. J. Gillihan The ICD-10 has similar diagnostic criteria but
Private Practice, Haverford, PA, USA identifies fewer subtypes.

https://doi.org/10.1007/978-3-031-14080-8_2
8 M. B. Powers et al.
Table 2.1 DSM-5 Diagnostic criteria for specific approximately 16%, with 0.6% reporting severe
phobia impairment (APA, 2013). Some of the higher
Pronounced fear or anxiety about a specific object or prevalence rates have been found in the United
situation (e.g., blood, animals, getting a shot). In States, but it is likely that these differences are a
children, the fear or anxiety may be expressed by
crying, tantrums, freezing, or clinging (criterion A) result of variations in assessment methods or cul-
The phobic object or situation almost always causes tural differences (Wardenaar et al., 2017). Along
fear or anxiety immediately following exposure with generalized anxiety disorder and separation
(criterion B) anxiety disorder, specific phobias are one of the
The phobic object or situation is avoided or suffered more commonly diagnosed anxiety disorders in
through with intense fear or anxiety (criterion C)
children (Costello & Angold, 1995). Additionally,
The fear or anxiety is disproportionate to the actual
danger presented by the specific object or situation Costello and Angold (1995) found that specific
and to the sociocultural context (criterion D) phobias in a community sample occur more fre-
The symptoms are not transient lasting 6 months or quently without comorbid diagnoses than any
more (criterion E) other anxiety disorder in children. Community
The fear, anxiety, or avoidance causes clinically samples have also shown that adults with a spe-
significant distress or disability in important areas
of functioning (e.g., social, education, development) cific phobia are significantly more likely to have
(criterion F) had a specific phobia as an adolescent but no
Difficulties are not better explained by symptoms of other previous anxiety diagnoses (Gregory et al.,
another mental disorder, including fear, anxiety, and 2007).
avoidance of situations associated with panic like or
other embarrassing or incapacitating symptoms (as
in agoraphobia), obsession-related objects or Comorbidity Clinical samples have shown dif-
situations (as in obsessive-compulsive disorder), ferent rates of co-occurring anxiety and internal-
traumatic event reminders (as in posttraumatic izing disorders in children. A sample of children
stress disorder), separation from home or
attachment figures (as in separation anxiety
referred to an outpatient anxiety center showed a
prevalence rate of 15% with specific phobia as
disorder), or social situations (as in social anxiety
disorder) (criterion G) the primary diagnosis; 64% of children with a
Note: Adapted from American Psychiatric Association primary specific phobia met diagnostic criteria
(2013, pp. 197) for a secondary diagnosis (Last et al., 1987b). A
similar study found that 72% of children between
Avoidance behaviors in children often take the the ages of 6 and 16 years, who were referred to
form of tantrums, crying, anger attacks, clinging, a phobia treatment clinic, had at least one comor-
and hiding. When the feared stimuli are present, bid diagnosis (Silverman et al., 1999). Some of
the severity of the fear response and avoidance the more common comorbid conditions included
behaviors indicate the extent of the child’s dis- an additional specific phobia (19%), separation
tress. Often the child is brought in for treatment anxiety (16%), and ADHD (6%) (Silverman
not because of the fear itself but rather due to et al., 1999). Additionally, there has been some
severity of the disruption to the family’s daily evidence that phobias, specifically fears of the
routine as a result of the avoidance and distress- dark, in children and adolescents increase the
related behaviors. likelihood of a co-occurring major depressive
disorder (Pine et al., 2001). Literature has also
demonstrated specific phobias in children can be
Epidemiology a predictor of later internalizing disorders, par-
ticularly if there are multiple phobias present (de
Prevalence In international community sam- Vries et al., 2019). For example, a retrospective
ples, the prevalence rate for specific phobias in study showed that out of participants who
children is 2.6–9.1% with the average near 5% reported childhood-specific phobias with one or
(Ollendick et al., 2002; APA, 2013). In 13- to more subtypes, lifetime prevalence of an inter-
17-year-olds, however, the prevalence rate is nalizing disorder was 46.3%; comparatively,
2 Issues in Differential Diagnosis: Phobias and Phobic Conditions 9
those without childhood phobias had a preva- age of onset (Stinson et al., 2007); however, there
lence of 18.2%, while those with four or more is a paucity of longitudinal research beginning in
phobia subtypes had an increased prevalence of early childhood. A meta-analysis (Lijster et al.,
75.6% (de Vries et al., 2019). 2016) revealed specific phobia had a mean onset
at 11 years of age. This, along with separation
Cultural differences The prevalence for specific anxiety and social phobia, is significantly earlier
phobias has been reported to be higher in African- than other anxiety disorders which begin, on
American children as compared to white children average, between 21.1 and 34.9 years of age
(Last & Perrin, 1993); however, rates may vary (Lijster et al., 2016). Other studies have reported
due to differences in specific phobia domains. even earlier age of onset around 7 and 8 years of
Fears indicated by African-American young age (Kessler et al., 2005; Wardenaar et al., 2017),
adults differ from their Caucasian American often ranging across specific phobia domains.
counterparts, with the former endorsing more For instance, animal, environmental, and blood-
specific phobias (Chapman et al., 2008). Mexican injection-injury phobias typically begin in early
American adults born in the USA also report childhood (Kessler et al., 2005; Wittchen et al.,
higher rates of specific phobia when compared to 1999), while situational phobias may start much
immigrant Mexican Americans as well as native later (Becker et al., 2007). Furthermore, several
non-Hispanic whites (Karno et al., 1989). There studies (Burstein et al., 2012; de Vries et al.,
have also been higher rates of specific phobias 2019) demonstrate that individuals who present
reported in Brazil than in the USA (Da Motta with multiple types of phobias at an early age
et al., 2000). Lower risk for specific phobias has experience increased severity and impairment
been reported among Asians and Hispanics and have higher rates of additional psychiatric
(Stinson et al., 2007) as well as in Japan disorders. Considering its early onset and high
(Kawakami et al., 2005) compared to Western psychiatric comorbidity rates, specific phobia
countries. In a study of children and adolescents may be a useful indicator for subsequent psycho-
in Seoul, Korea, the prevalence rate reported was pathology (Wittchen et al., 2003).
7.9% (Kim et al., 2010). In Uganda, the preva-
lence rate was much higher at 15.8%, with the Research on gender effects in children with
highest rates in children under 5 years of age specific phobias has generally shown few signifi-
(Abbo et al., 2013). A number of factors include cant differences under the age of 10 years (Strauss
operational definitions, ages sampled, and the & Last, 1993). According to the DSM-5, females
manner and content in which specific phobias experience specific phobia twice as frequently as
present may contribute to differences in sampling males (Bekker & van Mens-Verhulst, 2007),
and bias. Lastly, research including children in although this varies by phobia type. Literature on
non-Western countries remains sparse, making it gender differences has remained mixed, though
difficult to determine whether these results reflect most support a higher prevalence in females than
methodological differences or a true cultural dis- males (Beedso-baum et al., 2009; Fredrikson
parity. Diagnostic criteria in the DSM-5 address et al., 1996). For instance, a German study with a
cultural differences by stipulating that the fear community adolescent sample found that more
and anxiety caused by the specific phobia must girls than boys were diagnosed with specific pho-
be out of proportion to the sociocultural context bia (Essau et al., 2000). Researchers have posited
(APA, 2013). that this gender distinction may follow differ-
ences in how boys and girls are socialized and
Age and gender differences The prevalence of how the expression of fear is often viewed as
specific phobias tends to be higher in children more acceptable from females than males (Kane
and adolescents than in adults (Emmelkamp & et al., 2014). Strauss and Last (1993) have also
Wittchen, 2008). Most adults who meet diagnos- suggested that this gender disparity may be either
tic criteria for a specific phobia report an early based on methodological variations or a reflection
of the different rates of referral for treatment in (LeBeau et al., 2010), many researchers assert
boys versus girls. the number of specific phobias present is more
Despite the varied results of gender preva- predictive of severity and impairment (Burstein
lence across studies, there have been some con- et al., 2012; Stinson et al., 2007), regardless of
sistent findings related to gender differences the domain.
across subtypes of phobias. The DSM-5 indicates
higher rates of females than males experience
animal, environment, and situational-specific Structure of Fear
phobias, while blood-injection-injury phobia
affects both males and females equally. A study (Cox et al., 2003) using both exploratory
Environmental phobias tend to have an earlier and confirmatory factor analyses examined the
age of onset in boys (Wittchen et al., 1999), but factor structure of all specific phobia domains
are overall more prevalent in females (Beesdo- and found the following elements:
baum et al., 2009). Animal phobias are also more
common in girls with a 3:1 ratio clearly present • Agoraphobia: Public places, crowds, being
by age 10 years (Wittchen et al., 1998a, b). away from home, travel by car, train, or bus
Craske (2003) described adolescence as a period • Speaking: Public speaking, speaking to a
during which women develop fears and phobias group, talking to others
more rapidly than men do. McLean and Anderson • Heights/water: Flying, heights, crossing a
(2009) posit that this may be attributed to the bridge, water
effects of gender socialization during adoles- • Being observed: Public eating, public toilet
cence, where boys are encouraged to face their use, writing in front of others
fears, whereas girls are permitted to avoid them. • Threat: Blood/needles, storms/thunder,
Whatever factors contribute, it is clear that gen- snakes/animals, being alone, enclosed spaces
der differences in prevalence rates of specific
phobia become apparent during adolescence Higher-order analyses showed two second-
(Craske, 2003). order factors: social fears and specific fears.
Another factor analytic study of specific pho-
Specific phobias and subtypes Some of the bia subtypes used data from a large sample of
more commonly occurring phobias in children young adults from 11 countries. Results of this
include fear of heights, darkness, injections, study supported blood-injection-injury phobia
dogs, loud noises, small animals, and insects and animal phobia as two of the major classes of
(Essau et al., 2000; King, 1993; Silverman & fears across cultures (Arrindell et al., 2003).
Rabian, 1993; Strauss & Last, 1993). However, Environmental (e.g., storms, heights) and situa-
there have been few studies specifically examin- tional (e.g., flying, elevators) phobias were
ing the prevalence of subtypes, and most studies grouped together on one factor in this sample.
have focused on adult populations. Most recently, Additional studies have found similar results sug-
the National Epidemiological Study on Alcohol gesting that there may be few differences between
and Related Conditions found that fear of ani- environmental and situational phobias
mals and heights were the most commonly (Fredrikson et al., 1996). While these studies
reported phobias among adults, comprising more have been primarily with adults, there has been
than half of the diagnosed cases of specific pho- some research specifically examining children.
bia. This observation is consistent with Stinson Muris et al. (1999) found similar results in a sam-
et al.’ (2007) finding that animals are among the ple of children, indicating that environmental and
more commonly feared stimuli in children, situation types of phobias tend to cluster together
whereas blood-injury-injection phobias are in factor analyses. In a study examining mental
among the least common. While much attention disorders on a three-factor model consisting of
is placed on the subtype of specific phobia “anxious-misery,” “fear,” and “externalizing,”
Wittchen et al. (2009) discovered that animal and et al. (2013) go on to suggest that unique environ-
natural environment subtypes were routinely mental factors (i.e., individual events) account
attributed to the same factor, while blood-injury- for most of the variance beyond genetic factors,
injection subtype could not be precisely assigned whereas common environmental factors (i.e.,
to a single factor. These consistent results across events affecting multiple individuals) only con-
samples indicate that phobia subtyping may need tribute a small effect on variance.
to be refined. While there has been a range of results found
for the heritability of specific phobias, the herita-
bility of anxiety more generally has been demon-
Genetic Patterns strated consistently in the literature. Fyer et al.
(1995) found moderate aggregation for specific
There has been some evidence in family studies phobias in families where one family member
of a moderate degree of concordance for specific had an anxiety disorder. Hettema et al. (2001)
phobia diagnosis among family members. found similar results in a meta-analysis of the
Another consistent finding has been the relation- heritability of anxiety disorders in both family
ship between the fears of a mother and her child and twin studies. Hettema et al. (2005) examined
(Emmelkamp & Scholing, 1997). For example, anxiety disorders in a community sample of
mothers who fear insects may also have children twins and determined that for all the anxiety dis-
who exhibit fear in the presence of insects. While orders there appears to be two genetic factors that
there are a variety of factors such as temperament contribute to the development of symptomology.
and modeling that may contribute to the familial One of these factors is specifically associated
relationship among anxiety disorders, genetic with situational and animal phobias but no other
factors may also be responsible for some of the forms of anxiety. Because these two subtypes of
co-occurrence of this diagnosis. phobias are loaded together but separate from
Bolton et al. (2006) studied over 4500 6-year- other forms of anxiety, it suggests that there may
old twins to determine genetic and environmental be a unique genetic factor related to the develop-
influences on the development of early-onset ment of these two specific types of phobia mak-
anxiety disorders. For specific phobias, the heri- ing them distinct from the etiology of other forms
tability was around 60% with the remaining 40% of anxiety. Additional evidence has shown that
of variance attributed to differences in environ- individuals with the blood-injection-injury sub-
ment. As this study was conducted on young chil- type of specific phobia have more relatives with
dren and differs in results from other studies done similar problems indicating that this subtype may
on older children or adults, it is likely that early- be a separate category (Marks, 1987; Öst, 1992).
onset phobias may be more genetically deter- A more recent meta-analysis examined five stud-
mined than those developing later in childhood or ies and largely found similar results to previous
adulthood (Bolton et al., 2006). These findings literature (Van Houtem et al. (2013). The herita-
provide support for a non-associative model of bility rate range was 28–63% for blood-injury-
phobias which suggests an evolutionary basis to injection phobias, 22–44% for animal phobias,
fears rather than a conditioned fear model 0–41% for miscellaneous phobias, and 0–33%
(Menzies & Clarke, 1995). Another study exam- for situational phobias (Mean = 33%, 32%, 25%,
ining heritability of specific phobias used a sam- and 25%, respectively). The presence of unique
ple of 319 sets of twins between the ages of 8 and physiological attributes in blood-injection-injury
18 (Stevenson et al., 1992). The results of this phobia, including the risk for fainting which is
study suggested that differences in genes rare in other phobia subtypes (Connolly et al.,
accounted for 29% of the variance in specific 1976), also supports differentiating this subtype
phobia diagnosis, with shared and non-shared from other specific phobia subtypes.
environmental factors each accounting for a Contrary to the above results, the VATSPSUD
remaining third of the variance. Van Houtem study (Kendler & Prescott, 2006) found the
lowest rates of specific heritability for blood- those having a single phobia (Bianchi & Carter,
injection-injury phobias (7%). That is, those with 2012).
a relative with this specific type of phobia are not Despite the general conception that disgust
as likely to inherit that particular phobia. Kendler sensitivity is a genetically based vulnerability,
and Prescott (2006) also found similarly low there is little evidence of a genetic component.
rates for the specific heritability of situational Correlations in twin studies have shown very
phobias (15%). However, this study did find small genetic contribution (r = 0.29 for monozy-
common genetic factors contributing to all pho- gotic twins and r = 0.24 for dizygotic twins;
bias, with the largest contribution for animal Rozin et al., 2000). While a significant relation-
(21%) and blood-injection-injury (22%). ship exists between parent and child levels of dis-
gust (r = 0.52; Rozin et al., 2000), there are
environmental factors that could be contributing
Disgust Sensitivity to this relationship other than genetics.
Additionally, some researchers have suggested
Disgust sensitivity refers to the propensity for that gender differences in specific phobias may
experiencing disgust in a wide variety of set- be related to gender differences in disgust sensi-
tings. This sensitivity has been proposed to con- tivity (Davey, 1994). While early studies have
tribute to the development of a variety of been inconclusive, a recent study (Connolly
disorders particularly blood-injection-injury et al., 2008) found that disgust sensitivity medi-
phobias, animal phobias, and obsessive- ated the association between gender and specific
compulsive disorder (OCD; Olatunji & Deacon, phobias.
2008). Individuals with phobias related to spi-
ders frequently report feelings of disgust rather
than fear (Davey, 1992). In fact, disgust responses Social Anxiety Disorder (Social
to images of spiders have been shown to be pres- Phobia)
ent even when fear is not present (Olatunji,
2006). While little research has examined dis- Description
gust responses to in vivo spider exposure, people
with spider phobias report more disgust than Social anxiety disorder (social phobia) is charac-
non-phobic individuals (e.g., Olatunji & Deacon, terized by intense fear or discomfort in social
2008). There is also some evidence that disgust, situations. This fear can be limited to one specific
more so than anxiety, is a better predictor of situation (e.g., eating in front of others) or it can
avoidance of spiders (Olatunji & Deacon, 2008; be generalized to all social settings. Individuals
Woody et al., 2005). There are a few studies sug- with this type of anxiety fear embarrassment in
gesting that disgust sensitivity may be related these situations which often includes fear of
more to concerns about cleanliness and potential being ridiculed, laughed at, or disliked by peers.
for disease rather than concern related to physi- Individuals often have an overestimated percep-
cal harm in the presence of spiders and other tion of how anxious they appear physically. In
small animals and insects (Davey, 1992; Olatunji children, symptoms must persist for at least
& Deacon, 2008). Disgust sensitivity has also 6 months and must result in significant interfer-
shown to be significantly associated with certain ence in the child’s social functioning. In addition
psychopathological symptoms in children, to these criteria, the DSM-5 (pp. 202–208)
including blood-injection-injury phobia, animal requires the following:
phobia, and agoraphobia (Muris et al., 2008).
There is evidence that having both spider and • Marked fear or anxiety about one or more
blood-injection-injury phobias may have a com- social situations in which the individual is
pounding effect, such that people with both to exposed to possible scrutiny by others.
exhibit greater disgust sensitivity compared to Examples include social interactions (e.g.,
having a conversation, meeting unfamiliar anxiety disorder in childhood are less likely to
people), being observed (e.g., eating or drink- have problems with substance use in later adoles-
ing), and performing in front of others (e.g., cence (Kendall et al., 2004). Children with a pri-
giving a speech). *Note: In children, the anxi- mary anxiety disorder (including social anxiety
ety must occur in peer settings and not just disorder) are also at a much higher risk for OCD
during interactions with adults. and mood disorders, such as MDD or dysthymic
• The individual fears that he or she will act in a disorder (now persistent depressive disorder;
way or show anxiety symptoms that will be Waite & Creswell 2014) and educational prob-
negatively evaluated (i.e., will be humiliating lems, including decreased academic performance
or embarrassing; will lead to rejection or and early discontinuation (Kerns et al., 2013),
offend others). particularly in later adolescence (Kessler et al.,
• The social situations almost always provoke 1995). These heightened risks could be explained
fear or anxiety. *Note: In children, the fear or by consistent negative self-perceptions (Alfano
anxiety may be expressed by crying, tantrums, et al., 2006).
freezing, clinging, shrinking, or failing to
speak in social situations.
• The social situations are avoided or endured Epidemiology
with intense fear or anxiety.
• The fear or anxiety is out of proportion to the The lifetime prevalence of social phobia in an
actual threat posed by the social situation and adolescent population has been reported as 1.6%
to the sociocultural context (Essau et al., 1999b), although more recent litera-
• The symptoms are not transient lasting 6 months ture has suggested the lifetime prevalence rates to
or more. be higher, between 4.20% for men and 5.67% for
women (Clauss & Blackford, 2012). A meta-
For children and adults alike, the fear or anxi- analysis reported social anxiety disorder preva-
ety is considered excessive in relation to the lence in 28 countries to be 4.0% (Stein et al.,
actual threat posed by the social situation. In chil- 2017). The 12-month prevalence rate in US chil-
dren, these symptoms must be present in social dren is approximately 7% and is comparable to
situations involving similarly aged peers and not the rate among adults (APA, 2013). Prevalence
only around adults. In addition, the child must rates of social phobia in children in the general
demonstrate the capacity to engage in age- population range from 1% to 6% (Verhulst et al.,
appropriate social interactions with individuals 1997), although, again, more recent reviews have
with whom the child is familiar. The distress and suggested the rates to be higher, between 9.1%
avoidance seen in social settings is often demon- (Xu et al., 2012) and 12.1% (Ruscio, 2008). One
strated in tantrums, crying, clinging to caretakers, possible reason for this large range in prevalence
and hiding. Moreover, the fear and avoidance rates is the way certain forms of social anxiety
situations or objects experienced by children tend are coded by researchers. For example, both
to be narrower in range compared to those expe- school phobia and fear of public speaking could
rienced by adults (APA, 2013). be classified under either social anxiety or spe-
Social phobia in children and adolescents is cific phobia. Different studies have chosen to cat-
associated with a number of long-term negative egorize these types of fears differently which
outcomes. Children and adolescents with social may contribute to the inconsistent prevalence
phobia are at a high risk for developing substance rates across studies. In a more recent study con-
use earlier than their peers and tend to have a ducted with 8- to 13-year-olds in Norway, 2.3%
shorter interval between first use of substances of all children were reported to have significant
and problems associated with substance use symptoms of social anxiety (Van Roy et al.,
(Marmorstein et al., 2010). There is some evi- 2009). The rates of social phobia among a clini-
dence that those who receive treatment for an cal population have been reported around 15%
(Last et al., 1987b). As with all anxiety disorders, evidence showing that it does occur in children
there is a high level of comorbidity in social pho- (Wittchen et al., 2008), the typical age of onset
bia with one sample reporting that 63% of chil- for panic disorder is late adolescence into adult-
dren with social anxiety had a comorbid anxiety hood (Kessler et al., 2005), and the prevalence
disorder (Last et al., 1987b). rate among children younger than 14 years old is
Additionally, there is some evidence of sociode- less than 0.4% (APA, 2013). For many individu-
mographic differences in the prevalence of social als with panic disorder, the first panic attack
phobia. Inconsistent findings have been reported occurred during a time of psychosocial stress
for gender differences in social phobia. One study (Craske, 1999).
of a clinical sample found that boys were more
likely to have social anxiety than were girls
(Compton et al., 2000), while other studies have Symptoms of Panic
found that up to 70% of clinical samples of social
phobia are females (Beidel & Turner, 1988). There According to DSM-5 (pp. 208), a panic attack is
has been little cross-cultural research or research an “abrupt surge of intense fear or intense dis-
related to racial background in social phobia. comfort that reaches a peak within minutes, and
There is some evidence, however, that European during which time four (or more) of the follow-
American children are more likely to report more ing symptoms occur: palpitations, pounding
symptoms of social anxiety than are African heart, or accelerated heart rate; sweating; trem-
American children in a community sample bling or shaking; sensations of shortness of
(Compton et al., 2000), but these findings have not breath or smothering; feelings of choking; chest
yet been replicated. Social phobia is correlated pain or discomfort; nausea or abdominal distress;
with individuals who are single, never married or feeling dizzy, unsteady, light-headed, or faint;
divorced, and without children (APA, 2013). chills or heat sensations; paresthesias (numbness
or tingling sensations); derealization (feelings of
unreality) or depersonalization (being detached
Panic Disorder from one-self); fear of losing control or ‘going
crazy’; and fear of dying” (Table 2.2).
Description In order for panic attacks to be considered part
of panic disorder, at least one must be followed
The hallmark symptom of panic disorder is the by a month or more of one or both of the follow-
presence of recurrent and unexpected panic
attacks that cause the individual great anticipa- Table 2.2 DSM-5 Symptoms of panic attacks
tory anxiety. Panic attacks themselves are brief
Palpitations, pounding heart, or accelerated heart rate
periods of numerous physiological symptoms Sweating
accompanied by intense fear. For a majority of Trembling or shaking
individuals experiencing panic disorder, there is Sensations of shortness of breath or smothering
also agoraphobic avoidance—that is, avoidance Feeling of choking
of situations from which escape might be diffi- Chest pain or discomfort
cult in the event of a panic attack. Panic disorder Nausea or abdominal distress
was once thought to be a disorder found only in Feeling dizzy, unsteady, lightheaded, or faint
adults and very rarely in adolescents. This notion Chills or heat sensations
Paresthesias (numbness or tingling sensations)
was based on the idea that there is a strong cogni-
Derealization (feelings of unreality) or
tive component to panic disorder that children depersonalization (feeling detached from oneself)
were incapable of experiencing (Nelles & Barlow, Fear of losing control or going crazy
1988). However, there is now a large body of evi- Fear of dying
dence showing that panic disorder does occur in Note: Adapted from American Psychiatric Association
children (e.g., Kearney et al., 1997). Despite the (2013, pp. 208)
ing: (1) persistent concern or worry about having disorder. The defining feature is “marked, or
another attack or their consequences (e.g., losing intense, fear or anxiety triggered by the real or
control, a heart attack, going crazy) and (2) a sig- anticipated exposure to a wide range of situa-
nificant maladaptive behavior change related to tions” (pp. 218). However, there remains some
having these attacks. In children, making a diag- overlap in symptoms and diagnostic criteria
nosis of panic disorder can be challenging as (Asmundson et al., 2014). A diagnosis of agora-
some of the fears may present differently. For phobia requires marked fear or anxiety about at
example, young children may report a fear of least two of five situations:
becoming ill without any clear physical symp-
toms reported. In older children, reports of anxi- • Using public transportation (e.g., automo-
ety about becoming sick are common, as are biles, buses, trains, ships, planes)
fears of uncontrollable vomiting. Only in adoles- • Being in open spaces (e.g., parking lots, mar-
cence do individuals tend to start reporting fears ketplaces, bridges)
related to specific physiological symptoms. • Being in enclosed spaces (e.g., shops, the-
Children and adolescents report many of the aters, cinemas)
same physiological symptoms as adults, such as • Standing in line or being in a crowd
heart palpitations, nausea, shakiness, dizziness, • Being outside of the home alone (DSM-5,
sweating, headaches, and chills or heat sensa- pp. 217)
tions (Masi et al., 2000; Essau et al., 1999a;
Kearney et al., 1997). Somatic symptoms are Generally, these “situations are actively
more common than cognitive complaints, which avoided, require the presence of a companion, or
are reported more frequently among adolescents are endured with intense fear/anxiety” (pp. 218).
than children (Moreau & Follett, 1993). Phobic avoidance may be motivated by unrealis-
Nevertheless, there is evidence that some chil- tic fears of the consequences of having panic
dren and adolescent experience cognitive symp- symptoms, particularly in situations where the
toms, such as the fear of dying, the fear of going person feels trapped or far from help. For chil-
crazy (e.g., “I feel I am losing control”), or deper- dren, commonly feared situations are being out-
sonalization/derealization (e.g., “I don’t know side the home and becoming lost (DSM-5,
who I am” or “I don’t know where I am”). Twin pp. 220). There are some concerns for children
studies have demonstrated that panic disorder is failing to meet the new DSM-5 criteria and not
moderately heritable with a concordance rate of receiving proper treatment, mainly due to crite-
73% among monozygotic twins compared to 0% rion A (requiring symptoms elicited from two or
in dizygotic twins (Perna et al., 1997). The more of the situations listed above; Cornacchio
Virginia Adult Twin Study of Psychiatric and et al., 2015). However, the result and impact of
Substance Use Disorders (2005) found a panic this needs to be researched further.
disorder heritability of 28%, revealing that envi-
ronmental factors also play a considerable role.
However, two recent genome-wide association Epidemiology
studies on panic disorders did not produce sig-
nificant associations (Na et al., 2011). Agoraphobia is diagnosed in about 1.7% of ado-
lescents and adults each year, with a “substantial
incidence risk in late adolescence and early
Agoraphobia adulthood” (DSM-5, pp. 219). In a study of US
adolescents, Roberts et al. (2007) found a 1-year
Description prevalence rate of 4.5% (significantly higher than
the rates found in adults). In fact, this study found
In the DSM-5, agoraphobia was designated as its that agoraphobia was the most frequent anxiety
own diagnostic category independent of panic disorder in their sample, although the prevalence
dropped to 1.6% when impairment was required Table 2.3 DSM-5 Diagnostic criteria for separation anx-
iety disorder
for a diagnosis. In a 2010 study of mental disor-
ders in US adolescents (aged 13–18), the lifetime Recurrent excessive distress when anticipating or
experiencing separation from home or major
prevalence of agoraphobia was 2.4%, with higher attachment figures occurs or is anticipated
rates for females than males (3.4% versus 1.4%) Persistent and excessive worry about losing major
(Merikangas et al., 2010). Wittchen et al. (2008) attachment figures or about possible harm to them,
examined the prevalence of agoraphobia in such as illness, injury, disasters, or death
German adolescents. Adolescents with panic dis- Persistent and excessive worry about experiencing an
untoward event (e.g., getting lost, being kidnapped,
order or panic attacks were only moderately having an accident, becoming ill) that causes
more likely to develop subsequent agoraphobia, separation from a major attachment figure
while the majority of adolescents meeting crite- Persistent reluctance or refusal to go to out, away from
ria for agoraphobia had never experienced a home, to school, to work, or elsewhere because of fear
panic attack. While cultural/racial groups do not of separation
Persistent and excessive fear of or reluctance about
seem to have different prevalence rates, cultural
being alone or without major attachment figures at
context is considered in the DSM-5 when deter- home or in other settings
mining if symptoms are “out of proportion to the Persistent reluctance or refusal to sleep away from
actual danger posed” (pp. 219). home or to go to sleep without being near a major
attachment figure
Repeated nightmares involving the theme of
separation
Separation Anxiety Disorder Repeated complaints of physical symptoms (such as
headaches, stomachaches, nausea, or vomiting) when
Description separation from major attachment figures occurs or is
anticipated
Separation anxiety disorder is a somewhat unique Note: Adapted from American Psychiatric Association
(2013, pp. 190–191)
diagnosis in that, up until the DSM-5, it was the
only anxiety disorder limited to children and ado-
lescents. Separation anxiety disorder is defined in • Persistent and excessive fear of or reluctance
DSM-5 (pp. 190) as “developmentally inappro- about being alone or without major attach-
priate and excessive fear or anxiety concerning ment figures at home or in other settings
separation from those to whom the individual is • Persistent reluctance or refusal to sleep away
attached, as evidenced by three or more of the from home or to go to sleep without being
following (Table 2.3): near a major attachment figure
• Repeated nightmares involving the theme of
• Recurrent excessive distress when anticipat- separation
ing or experiencing separation from home or • Repeated complaints of physical symptoms
from major attachment figures (such as headaches, stomachaches, nausea, or
• Persistent and excessive worry about losing vomiting) when separation from major attach-
major attachment figures or about possible ment figures occurs or is anticipated.”
harm to them, such as illness, injury, disasters,
or death To be considered clinically significant, these
• Persistent and excessive worry about experi- symptoms must be present in children and ado-
encing an untoward event (e.g. getting lost, lescents for at least 4 weeks. Comparatively,
being kidnapped, having an accident, becom- adults must present these symptoms for 6 or more
ing ill) that causes separation from a major months. Particular to children, the symptoms
attachment figure must be developmentally inappropriate for the
• Persistent reluctance or refusal to go to out, child’s biological age. Many of these symptoms
away from home, to school, to work, or else- would be considered developmentally appropri-
where because of fear of separation ate in children ages 7 months to 6 years old
(Bernstein & Borchardt, 1991), and thus it is Prevalence rates in community samples for
important to consider both age and developmen- separation anxiety disorder ranged from 2.0% to
tal level when making a diagnostic determina- 12.9% (Anderson et al., 1987; Kashani &
tion. The underlying fear found in separation Orvaschel, 1988; McGee et al., 1990). Among
anxiety disorder is an exaggerated fear of losing children 12 years old and younger, separation
or becoming separated from parents or other pri- anxiety disorder is the most prevalent disorder
mary caregivers. In addition to these fears, many and has been found to decrease throughout the
children experience nightmares related to becom- lifespan (APA, 2013), consistent with previous
ing separated from caregivers (Bell-Dolan & literature. The range in rates may be attributable
Brazeal, 1993). to the age at which symptoms were assessed.
Symptom differences have been found The lower rates of prevalence were found in
between ages but not between genders (Francis studies examining adolescents, while the higher
et al., 1987; Paulus et al., 2015). Young children rates were found in community samples of
(ages 5–8 years) are most likely to report fears of younger children. Rates among clinical popula-
harm to self or caregivers, nightmares, and school tions are higher than the general population,
refusal. Children between the ages of 9 and with 33% of a sample of anxious children meet-
12 years present with more excessive distress at ing diagnostic criteria for separation anxiety
the time of separation, while adolescents are disorder (Last et al., 1987b). Results of this
more likely to experience somatic symptoms and study also indicated that 41% of the children
school refusal. Similarly, children tend to exhibit with a primary diagnosis of separation anxiety
physical symptoms such as headaches and nau- disorder had a comorbid anxiety diagnosis, the
sea, whereas adolescents and adults tend to expe- most common being GAD or specific phobia
rience cardiovascular symptoms (APA, 2013). (APA, 2013).
Some children have also described perceptual A number of sociodemographic variables
experiences. Additionally, older children and have been associated with separation anxiety
adolescents are most likely to experience a disorder. Most samples examining separation
smaller number of symptoms than are younger anxiety disorder have been primarily with chil-
children. dren of European descent, although this find-
ing may reflect biased sampling rather than
true cultural differences (Strauss & Last,
Epidemiology 1993). However, one study in Uganda found a
child/adolescent prevalence rate of 5.8% (Abbo
While separation anxiety disorder can present in et al., 2013). As with most other anxiety disor-
children of all ages, it is most common in preado- ders, rates of separation anxiety disorder are
lescent age ranges. Typically, the onset is acute higher in females than males (Compton et al.,
and follows a significant change in the child’s life 2000); however, there is evidence of equal
(e.g., start of school, moving, death of a parent or rates in a clinical sample (APA, 2013).
close relative) or developmental changes (Last, Contrarily, a few published reports found no
1989). Several studies have shown that separation gender differences (Bird et al., 1989; Last
anxiety disorder follows an intermittent course et al., 1992; Paulus et al., 2015). Additionally,
over time. Children often experience remissions lower SES and parental education levels have
and relapses around times of school holidays, been associated with higher rates of separation
vacations, and life stressors (Cantwell & Baker, anxiety disorder in children (Bird et al., 1989;
1988; Hale et al., 2008). When followed over a Last et al., 1987b). In a study examining sepa-
period of 4 years, 96% of children initially diag- ration anxiety disorder heritability, researchers
nosed with separation anxiety disorder no longer estimated a heritability rate of 73% in a com-
met diagnostic criteria, the highest recovery rate munity sample of 6-year-old twins (Bolton
of any anxiety disorder studied (Last et al., 1996). et al., 2006).
Role of Avoidance Differential Diagnosis
In addition to the many fears that children with evelopmentally Appropriate Fear
D
separation anxiety disorder experience, the Versus Anxiety Disorders
avoidance of situations is a key element of this
disorder. Additionally, avoidance behaviors An important diagnostic issue to consider in chil-
play an important sustaining role in anxiety dis- dren is whether the anxiety is developmentally
orders (Foa & Kozak, 1986). There is a large appropriate or is part of a disorder. Anxiety and
range of avoidance behaviors common to chil- its various associated physiological symptoms
dren with separation anxiety disorder, and types are considered to be basic human emotions
of avoidance may vary by age. Reluctance to be (Barlow, 2002). In young children, common
being alone or without an adult and reluctance developmental fears include fear of the dark, fear
to sleep away from caregivers or from home are of new situations including the first day of school,
the most frequently reported avoidance behav- fear of separation from parents or other caretak-
iors (Allen et al., 2010). Milder forms of avoid- ers, and fear of large animals. In adolescents,
ance include hesitation to leave home, common developmental fears include anxiety
requesting that the caregiver be accessible via related to job interviews, college applications,
phone during outings, and frequent questions and dating.
about schedules. More moderate forms of An important distinction between develop-
avoidance in younger children can include mentally appropriate fears and phobias is both
clingy behaviors with parents or caregivers the duration and severity of the anxiety. For the
(e.g., following the adult around the house). anxiety to become clinically significant, it must
Older children may be more likely to have dif- persist for a period of at least 6 months and
ficulty leaving home without caregivers or include significant avoidance and interference in
refuse to participate in social activities with daily functioning (Albano et al., 2001). While
peers if the caregiver is not present. More seri- this distinction often is based on clinical judg-
ous forms of avoidance can include faking ill- ment, there has been research showing that a spe-
nesses, school refusal, or refusal to sleep alone cific phobia diagnosis can be reliably achieved
at night. According to the DSM-5 (2013), girls through the use of structured clinical interviews
may exhibit more reluctance or avoidance to and standardized self-report measures (Schniering
attend school than boys. et al., 2000). One common assessment used for
Avoidance behaviors may slowly increase the diagnosis of anxiety disorders in children is
over time. Albano et al. (2003) describe a pattern the Multidimensional Anxiety Scale for Children
of increasing avoidance that starts with occa- Second Edition (MASC; March et al., 1997;
sional nightmares and subsequent requests to March, 2012). This self-report scale is used to
sleep with parents. From this relatively mild differentiate clinical from nonclinical samples as
behavior change, the child can become increas- well as distinguish different forms of anxiety. It
ingly avoidant until he or she is sleeping with has been found to be sensitive to the differences
one or both parents every night. Similarly, in these groups (Dierker et al., 2001). The Anxiety
Livingston et al. (1988) describe a pattern of Disorders Interview Schedule for Children
increasingly serious physical complaints on the (ADIS-C; Silverman & Albano, 1996) is another
part of the child. This behavior often progresses useful structured interview for diagnosis of
from very vague complaints of not feeling well anxiety disorders in children. The updated ADIS-
to frequent complaints of stomachaches or head- 5-
C/P is under development. The structured
aches. It is often these avoidance behaviors that Clinical Interview for DSM-5 (SCID-5) specifi-
will prompt the parent to bring the child in for cally tailored for children and adolescents is also
treatment. currently under development.
istinguishing Between Different

D develop a panic attack, when confronted with the
Anxiety Disorders feared stimuli. The presence of panic attacks is
not sufficient to warrant the diagnosis of panic
Given the substantial overlap in symptoms across disorder, given that only a small minority of indi-
the disorders presented in this chapter, it may be viduals who experience panic attacks go on to
difficult at times to identify which diagnosis a develop panic disorder; results from the National
given child’s symptom presentation warrants. Comorbidity Survey Replication revealed a
The task can be all the more challenging in light 22.7% lifetime prevalence estimate for panic
of children’s difficulty at times in reporting attacks versus a 3.8% rate for panic disorder
clearly what they are experiencing. Even if they (Kessler et al., 2006, 2012). Specific phobia is
are willing to discuss their experiences, there indicated when the child’s fear, including panic
may be limitations in their vocabulary or concept attacks, is provoked by the phobic stimulus
formation to fully describe their fears. Accurate itself—for example, a dog. The content of the
diagnosis is important for case conceptualization fear in this case would have to do with the possi-
such that the most appropriate treatment can be bility of injury as a result of contact with the dog.
administered. For example, a cognitive-At the core of panic disorder, on the other hand,
behavioral clinician would expose an individual is a fear of the panic attacks themselves (the so-
with panic disorder to interoceptive cues (e.g., called “fear of fear”; e.g., Chambless et al.,
pounding heart) but would follow a different 1984).
treatment plan for an individual with separation
anxiety disorder. The following section covers Differential diagnosis can be more difficult
common distinctions that must be made in the when the feared stimulus or situation is one that
differential diagnosis of specific phobia, social commonly is associated with panic disorder—for
phobia, panic disorder, agoraphobia, and separa- example, a fear of elevators. In these cases, it is
tion anxiety disorder. In most cases, the correct imperative that the diagnosing clinician ascertain
diagnosis can be derived by understanding what whether the patient is afraid of panicking in these
is at the core of the patient’s fears. situations or simply is afraid of the situations
themselves (e.g., fears that the elevator will fall).
Specific phobia vs. social phobia Of the disor- Finding that the individual fears several situa-
ders under consideration, the two that share the tions that provoke panic attacks (e.g., car trips,
most symptom criteria may be the most straight- elevators, crowds) makes a diagnosis of panic
forward to distinguish based simply on the con- disorder more likely than diagnosis of a specific
tent of the fears. Specific and social phobia phobia to multiple situations.
overlap in nearly all of their diagnostic criteria
except that social phobia involves a fear of social Specific phobia vs. separation anxiety disor-
situations (e.g., talking to a group, answering der Specific phobia and separation anxiety dis-
questions in class), whereas specific phobia order both may include significant levels of
involves a fear of other stimuli. In cases where avoidance. The primary distinction between these
the distinction may be somewhat difficult—for disorders is based on whether the avoidance is
example, fear of clowns—the differential diagno- driven by fear of the avoided stimulus, as in
sis is based on whether the fear is primarily social specific phobia, or by fear of separation from
(e.g., being publicly embarrassed by the clown) attachment figures, which defines separation anx-
or involves fear of the stimulus itself (e.g., being iety disorder. Although children with specific
attacked by the clown). phobia may cling to their caregivers when con-
fronted with the phobic stimulus, the clinging
Specific phobia vs. panic disorder Children behavior represents the child’s looking to the
with specific phobias often will experience many caregiver for safety and protection. In contrast,
physiological symptoms of panic, and may even the core fear in separation anxiety disorder is
separation from the caregiver in and of itself. For blush. In this case, the child will fear the social
this reason, the fear of separation is likely to be situation itself, not their possible public panic
more pervasive than in specific phobia in which response.
fear of separation is provoked by the presence of
a relatively limited range of stimuli (e.g., dogs). Social anxiety disorder (social phobia) vs. sepa-
ration anxiety disorder As with panic disorder,
Specific phobia vs. agoraphobia Specific pho- separation anxiety disorder can also resemble
bia and agoraphobia share similar criteria, par- social anxiety disorder in some respects. For
ticularly regarding feared situations. DSM-5 example, school refusal may be driven by social
guidelines state that if the individual fears one anxiety or by the distress associated with separa-
situation, specific phobia should be considered, tion from one’s caregiver. Careful questioning of
as agoraphobia requires two or more feared situ- the child and, if necessary, the parents may reveal
ations. Additionally, the motive for the feared the underlying fear. Whereas social anxiety dis-
situation is an important factor in distinguishing order is characterized by the fear of being judged
the two diagnoses. For example, an individual negatively by others, separation anxiety is defined
who displays crowd phobia tendencies due to by the fear of being separated from attachment
fear of being harmed may be diagnosed with spe- figures (APA, 2013). For example, if the child has
cific phobia, whereas an individual who fears no trouble socializing with peers when the par-
crowds due to fear of displaying panic-like symp- ents are present but refuses to go to school,
toms would be appropriate for an agoraphobia sleepovers, and other events where the parents
diagnosis. are not present, a diagnosis of separation anxiety
disorder is likely. On the other hand, if the child
Social anxiety disorder (social phobia) vs. panic is still terribly afraid of social settings even in the
disorder A child who presents with panic attacks presence of the parents, the accurate diagnosis is
and a fear of social situations could be living with likely social anxiety disorder.
either panic disorder or social anxiety disorder.
Additionally, both conditions lead to avoidance Social anxiety disorder (social phobia) vs. ago-
of social situations, such as school refusal. raphobia The main factor differentiating social
Indeed, the Panic Appraisal Inventory (Telch, anxiety disorder from agoraphobia is the stimu-
1987), which is commonly used to measure lus triggering symptoms and the cognitive ide-
panic-related concerns, comprises a subscale of ation (DSM-5). A diagnosis of agoraphobia will
panic consequences that include social concerns. be defined by marked by fear, anxiety, and avoid-
Though frequently co-occurring (Schneier et al., ance of certain places or situations. Conversely,
1992), social anxiety disorder and panic disorder fear of negative evaluation will be at the core of a
can be distinguished by the primary fear driving social anxiety disorder diagnosis.
the anxiety. While social anxiety disorder is char-
acterized by fear of negative evaluation, panic Panic disorder vs. separation anxiety disor-
disorder is characterized by fear of the panic der The final differential diagnosis, between
attacks themselves (APA, 2013). For example, a panic disorder and separation anxiety disorder,
child may fear that they will panic in school, can be one of the more difficult distinctions to
faint, and have to be carried out of the classroom make. In fact, there is strong evidence that sepa-
while the whole class watches. In this case, the ration anxiety disorder is a risk factor for panic
child is unlikely to fear social situations per se, disorder (Kossowsky et al., 2013). Both disorders
but rather the possibility of having a panic attack may include clinging to “safe” persons, often the
in a social setting. Similarly, children with social parents. Once again, making the right diagnosis
phobia may fear embarrassing themselves in depends on identifying the child’s specific fear.
public due to their anxiety response—for exam- In panic disorder, the strong desire to be close to
ple, that they will shake, trip over their words, or a safe person is driven by fears related to panic—
for example, the person with agoraphobia who is orders is also in the excellent range (Brown et al.,
concerned that she will have a panic attack when 2001). The reliability of diagnosis specifically in
help is not available. In this case, the safe person children has also been found to be good when
provides a sense of comfort in the face of a poten- using structured diagnostic interviews
tial panic attack, similar to the function of having (Schniering et al., 2000). This high level of reli-
a bottle of benzodiazepines always nearby. With ability has improved the ease of communication
separation anxiety disorder, the fear is related to between mental health professionals about a
separation from the caregiver in its own right. given patient’s clinical status.
Unwanted separation from the caregiver may While there are positive aspects to the current
trigger a bout of anxiety that leads to a panic diagnostic system, there also are significant limi-
attack, but the root of the anxiety is the separation tations to the way disorders are defined. First,
and not the panic symptoms. many diagnoses contain words like “persistent,”
“clinically significant,” and “excessive” without
Panic disorder vs. agoraphobia Agoraphobia defining the threshold for such criteria. This
should only be diagnosed when avoidance behav- vagueness can lead to disagreement across clini-
iors associated with panic attacks extend to two cians. With respect to children specifically, the
or more agoraphobic situations. current DSM does not address developmental
norms that can be expected across ages. It also
Agoraphobia vs. separation anxiety disor- does not address how specific disorders may
der Much like with panic disorder, the differen- present themselves differently in different age
tiation between agoraphobia and separation groups. Therefore, the clinician often must make
anxiety disorder lies in the specific cognitive ide- a judgment call as to whether a particular behav-
ation. In agoraphobia, the focus is on panic-like ior falls outside the realm of developmentally
or other incapacitating or embarrassing symp- appropriate behavior in a child, creating a lack of
toms in feared situations, whereas the cognitive reliability in diagnosis. By improving this defini-
ideation in separation anxiety disorder is more tion, a clearer threshold would be established that
likely thoughts on detachment from parents or would ideally incorporate developmental norms
other attachment figures. for diagnosis in children. A clearer definition of
this threshold would dramatically improve diag-
nostic reliability as much of the lack of diagnostic
Diagnostic Reliability agreement in this area is caused by differing defi-
nitions of what is “developmentally appropriate”
In light of the often-challenging differential diag- (Albano et al., 2003).
nosis of the disorders described in this chapter, Second, diagnoses could be improved by
arriving at a reliable diagnosis is imperative to increasing the reliability of subtypes of specific
provide treatment recommendations. The current phobias. There is significant co-occurrence of
diagnostic system was adopted in an attempt to multiple subtypes in individuals diagnosed with
increase the reliability of diagnoses across clini- specific phobias and a lack of empirical support
cians. Attempts to determine diagnostic reliabil- for the current subtypes. Blood-injection-injury
ity often rely on test-retest or interrater reliability phobias seem to have both different physiologi-
approaches, including the audio/video-recording cal responses and psychometric properties and
method. Knappe et al. (2013) demonstrated high likely represent a clear subtype. However, the
test-retest reliability of the dimensional anxiety other subtypes do not seem to have the same psy-
scales, including social anxiety disorder, agora- chometric differentiation. As with social phobia,
phobia, and panic disorder. In accordance with it may make sense to refer to specific phobias in
previous research (Lebeau et al., 2012), Knappe terms of simple type (one specific phobia) and
et al. (2013) reported low test-retest reliability for generalized type (more than one specific phobia;
specific phobia. Interrater reliability for these dis- Piqueras et al., 2008).
Third, symptoms of panic disorder should DSM, changes in several areas of the system
more clearly be differentiated by age range. could lead to more reliable diagnosis and clearer
There is evidence that children of different ages differentiation between anxiety disorders.
report different types and numbers of symptoms.
This developmental variability needs to be
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Issues in Differential Diagnosis:
Considering Generalized Anxiety 3
Disorder, Obsessive-Compulsive
Disorder, and Posttraumatic Stress
Disorder
Nicole Fleischer, Jonathan Rabner,

Julia Spandorfer, and Philip C. Kendall
Introduction order also met criteria for an additional disorder

(Kendall et al., 2010). Differential diagnosis
As a rule, an accurate diagnosis provides a foun- among disorders (i.e., anxiety and related disor-
dation for case conceptualization and facilitates ders) poses challenges to both researchers and
effective treatment practices, and accurate diag- clinicians.
noses are critical to the organization of partici- The diagnostic assessment of children and
pants for empirical research. Although not adolescents carries with it additional consider-
without its own problems, the Diagnostic and ations not present when working with adults. For
Statistical Manual of Mental Disorders (DSM-5), example, DSM-5 identifies some developmental
currently in its fifth iteration (American differences in the diagnostic criteria for general-
Psychiatric Association, 2013), is the most fre- ized anxiety disorder: only one physical symp-
quently used taxonomic system for organizing tom is required for children and adolescents,
psychological disorders. Within this framework, whereas three physical symptoms are required
disorders are presented as categories (discrete for adults. When diagnosing obsessive-
entities) characterized by specific criteria. compulsive disorder, the criterion requiring that
Although specifying criteria is a decided compulsions be aimed at reducing distress is
improvement, one of the shortcomings of a cate- laxed for children. Additionally, separate criteria
gorical approach is the existence of considerable exist for diagnosing posttraumatic stress disorder
overlap in symptomatology among disorders. in children 6 years and younger. Thus, features
Indeed, comorbidity is common, and among that may serve to differentiate disorders among
youth with anxiety disorders, it is the norm adults may or may not apply to youth. Both chil-
(Kendall et al., 2001; Merikangas et al., 2010). dren and parents typically provide information
For example, in a large sample of 7–17-year-olds, about the presenting youth. However, the agree-
55% of youth who met criteria for an anxiety dis- ment between parent and child reports of anxiety
disorders is usually limited (Choudhury et al.,
N. Fleischer 2003; De Los Reyes, 2011). Clinicians can
Philadelphia College of Osteopathic Medicine, resolve this discrepancy by assigning a diagnosis
Philadelphia, PA, USA if the child meets criteria by either the child’s
J. Rabner · J. Spandorfer · P. C. Kendall (*) report or the parents’ report. Nevertheless, the
Temple University, Philadelphia, PA, USA reasons underlying parent–child discrepancies
e-mail: philip.kendall@temple.edu

https://doi.org/10.1007/978-3-031-14080-8_3
30 N. Fleischer et al.
may be important for case conceptualization and youths’ symptomatology within each domain
treatment and should not be overlooked (De Los will help our understanding. Next, the reliability
Reyes & Kazdin, 2005). For example, differences and validity of the diagnoses will be considered.
may be contingent upon the observability of the Last, this chapter will discuss current research
symptoms being reported (Comer & Kendall, findings in terms of their diagnostic
2004). Given the limited number of studies spe- implications.
cific to issues of differential diagnosis among
youth, the present discussion also draws upon
findings from the adult literature. That said, it is ssential Features of GAD, OCD,
E
clear that research is needed before conclusions and PTSD
can be drawn regarding differential diagnosis
among youth. Generalized Anxiety Disorder
This chapter addresses issues of differential
diagnosis pertaining to generalized anxiety disor- The hallmark of GAD is the presence of exces-
der (GAD), obsessive-compulsive disorder sive, uncontrollable, and persistent worry about a
(OCD), and posttraumatic stress disorder number of events or activities, more days than
(PTSD), with an emphasis on the potential diag- not for at least 6 months (APA, 2013). Worry has
nostic confusions among these three disorders. been defined as “a chain of thoughts and images,
As is often the case among psychological disor- negatively affect-laden and relatively uncontrol-
ders, GAD, OCD, and PTSD share similar symp- lable” (Borkovec et al., 1983, p. 10). For youth,
tom presentations. Perhaps most prominent, and these worries frequently concern health, school,
potentially most troublesome, all three disorders and personal harm (Silverman et al., 1995; Muris
are characterized by the presence of intrusive, et al., 2000) and must be associated with at least
repetitive cognition that causes distress. Among one physiological symptom (i.e., feeling keyed
adults and youth, it can be difficult to delineate up or on edge; being easily fatigued; difficulty
diagnostic boundaries. For example, a child may concentrating or mind going blank; irritability;
report that they frequently experience thoughts of muscle tension; or sleep disturbance). In addi-
their mother in a car crash. This presentation tion, the worry or physical symptoms must cause
could suggest worry regarding the safety of fam- distress or impairment in important areas of func-
ily members, obsessional thinking, or flashbacks tioning, which for youth often include school/
of an earlier trauma, corresponding to GAD, academics, peer relationships (i.e., Verduin &
OCD, and PTSD, respectively. How best to make Kendall, 2008), and family/home life.
sense of such a youth report? Critical to differential diagnosis, the focus of
This chapter will first provide a description of the anxiety and worry present in GAD cannot be
the essential diagnostic features of GAD, OCD, better accounted for by features of another disor-
and PTSD in youth along with a brief overview der. For example, if the excessive and interfering
of epidemiological findings. We then examine worry is entirely focused on peer evaluation,
specific areas of diagnostic overlap and confu- social anxiety disorder may be more apt than
sion. These domains are organized into five cate- GAD, or if the worry is solely about gaining
gories of symptoms: (1) fear/anxiety, (2) recurrent weight, a diagnosis of anorexia nervosa may be
thoughts, (3) intrusive images, (4) physical appropriate. In addition, the symptoms of GAD
symptoms, and (5) avoidance. These symptom must not be attributable to the effects of a sub-
domains are present in nearly every anxiety dis- stance or a medical condition.
order, help distinguish anxiety disorders from Onset of GAD in childhood does exist (e.g.,
other disorders, and may facilitate differential Kendall et al., 2010), but it is the case that the
diagnosis. Given the high rate of comorbidity, main incidence period for GAD is adolescence
symptom overlap, and heterogeneity within diag- and adulthood (Beesdo et al., 2010), with preva-
nostic categories, a nuanced examination of lence estimates in adolescence at about 3%
3 Issues in Differential Diagnosis: Considering Generalized Anxiety Disorder, Obsessive-Compulsive… 31
(Burstein et al., 2014). Onset of GAD is often tion disorder. Regarding differential diagnosis,
earlier in females than in males, with prevalence DSM-5 specifies that obsessions are not simply
estimates increasing with age in children and excessive worries about real-life problems, but
adolescents (Beesdo et al., 2009). Additional instead center around irrational, magical worries
research is needed to examine the gender ratio in (APA, 2013). The obsessions and compulsions
youth. cannot fall within the circumscribed content
domains of other anxiety or obsessive-compulsive
disorders. For example, obsessions related to
Obsessive-Compulsive Disorder one’s own appearance may better fall under the
diagnosis of BDD, and hair-pulling (not cos-
OCD is characterized by the presence of obses- metic) may be better accounted for by a diagnosis
sions or compulsions. Most individuals with of trichotillomania.
OCD experience both obsessions and compul- Similar to GAD, OCD likely develops between
sions, and the presence of pure obsessions is childhood and mid-adolescence, with the average
uncommon (APA, 2013; Foa et al., 1995). age of onset falling between 7.5 and 12.5 years
Obsessions are defined as recurrent and persis- (Geller et al., 1998). Several epidemiologic stud-
tent thoughts, impulses, or images that are intru- ies conducted with adolescents in the United
sive, inappropriate, and experienced as distressing States and elsewhere report prevalence rates
(APA, 2013). The most common obsessions ranging from approximately 2% to 4% of the
among clinically affected youth involve themes pediatric (Geller, 2006). Among clinic-referred
of contamination, harm or death, and symmetry youth, the lifetime prevalence rate is approxi-
(Hanna, 1995), though recent research demon- mately 15% (Last et al., 1992). The gender ratio
strates that children and adolescents may differ in is not clear in children: some data suggest that
presentations of obsessions, including an OCD is more common in boys (Geller et al.,
increased presentation of sexual obsessions in 1998; Zohar et al., 1997), whereas other data
adolescents (Selles et al., 2014). Youth with OCD indicate no difference in sex distribution (Anholt
often perform compulsions to ignore, hold back, et al., 2014; Chabane et al., 2005).
or neutralize obsessive thoughts and related feel-
ings. Compulsions are repetitive, intentional
behaviors performed to reduce anxiety or distress Posttraumatic Stress Disorder
and are often performed stereotypically or
according to rigid rules. Unlike adults, youth do PTSD is characterized by a constellation of
not have to recognize that the obsessions or com- symptoms that develop in response to a trauma.
pulsions are excessive or unreasonable. While Specifically, it can occur when an individual
children and adolescents do not necessarily differ experiences, witnesses, learns about a close fam-
in severity of symptoms, adolescents may experi- ily member or friend experiencing, or is repeat-
ence more control over compulsions (Selles edly exposed to as part of one’s job (school), an
et al., 2014). Given that intrusive thoughts and event involving actual or threatened death, seri-
images regularly occur in the general population, ous injury, or sexual violence (APA, 2013).
symptoms must be distressing, time consuming In DSM-5, PTSD was relocated to a new cat-
(lasting more than 1 h per day), or interfering egory, “Trauma and Stressor-related Disorders.”
with academic functioning, social activities, or Further, the DSM-5 includes separate diagnostic
relationships to warrant a diagnosis of OCD. criteria for PTSD for children and for adults older
The DSM-5 separates anxiety and obsessive- than six and children younger than six. For those
compulsive disorders, creating a separate cate- older than six, there must be at least one intrusion
gory of obsessive-compulsive disorders that symptom (e.g., recurrent distressing dreams), at
include OCD, body dysmorphic disorder (BDD), least one avoidance symptom (e.g., avoidance of
hoarding disorder, trichotillomania, and excoria- memories), at least two negative alterations in
cognitions and mood (e.g., distorted blame about much lower prevalence rate of 0.1% (Lavigne
the traumatic event, persistent negative emotional et al., 1996).
state), and at least two alterations in arousal and
reactivity (e.g., irritable behavior, hypervigi-
lance). The disturbance must last for longer than Domains of Symptom Overlap
1 month and cause meaningful distress or impair-
ment in important areas of functioning. For those Fear/Anxiety
younger than six, a lower threshold of symptoms
must be met, and there is a focus on observable All anxiety disorders are characterized by the
symptoms rather than reports on internal presence of fear or apprehension in some form,
experiences. and the presence of fear/anxiety can help differ-
A history of adverse or traumatic events can entiate anxiety disorders from other psychopa-
be present in individuals with diagnoses other thology, such as mood disorders. This domain
than PTSD. The stress associated with traumatic can include fear of specific stimuli, situations, or
events may serve as a catalyst for the manifesta- feelings. Fear of specific stimuli is characteristic
tion of an underlying vulnerability, as described of OCD and among the possible symptoms of the
in the diathesis-stress model. Thus, the presence disorder. It may also be present in GAD and
of a traumatic event is necessary but not suffi- PTSD, but it is not explicitly included as a symp-
cient for a diagnosis of PTSD. Moreover, differ- tom of the disorders. Likewise, fear of a specific
ential diagnosis was informed by the timing of situation (e.g., riding the bus) may be present in
symptom onset. As noted in DSM-5, symptoms GAD, OCD, and PTSD, requiring a more specific
of intrusion, avoidance, negative alterations of understanding of the fear. For example, a child
cognitions and mood, and alterations of arousal with GAD may fear that the bus will get lost or
and reactivity must begin or worsen after the will cause him to be late, whereas a child with
trauma. Based on this framework, symptoms of OCD may fear that every time the bus hits a bump
PTSD were distinguished from psychotic halluci- it is running over a person; a child with PTSD
nation, agoraphobia, specific phobia, and depres- may have previously been in a bus accident.
sion. Of course, the presence of PTSD does not An interesting notion is the “fear of fear” (e.g.,
exclude the presence of other disorders, as evi- fear of experiencing fear; Goldstein & Chambless,
denced by the high comorbidity rates of both 1978), sometimes referred to as anxiety sensitiv-
adults and children diagnosed with PTSD ity, that is often thought of as the signature fea-
(Salloum et al., 2018). ture of panic disorder, but it may also be present
Notably, not all youth who experience trauma in GAD (Knapp et al., 2016) and PTSD (Hensley
develop PTSD, and there is evidence to suggest & Varela, 2008; Viana et al., 2018). Individuals
that age, gender, and environmental factors all with heightened anxiety sensitivity evidence a
play a role in differential outcomes (e.g., Furr fear of physiological symptoms of anxiety due to
et al., 2010; Bokszczanin, 2007, 2008; McNally, the belief that those sensations are deleterious to
1993). Approximately 16% of children who are their physical, psychological, and/or social well-
exposed to a traumatic event develop PTSD being (Schmidt et al., 2010; Reiss & McNally,
(Alisic et al., 2014). A survey of adolescents in a 1985). In GAD, anxiety sensitivity has been asso-
population-based sample found a 4.7% preva- ciated with worry regarding uncertainty (Floyd
lence rate for PTSD, which was significantly et al., 2005). Regarding PTSD, anxiety sensitiv-
higher among females (7.3%) compared to males ity has been thought to be a vulnerability and
(2.2%; McLaughlin et al., 2013). While boys are maintenance factor (Elwood et al., 2009) and has
more likely to be victims of physical violence, been implicated as such in children and adoles-
girls are more likely to experience sexual vio- cents (e.g., Kiliç et al., 2008).
lence (McLaughlin et al., 2013). A large-scale Intolerance of uncertainty (IU) has been
survey of PTSD in children aged 2–5 revealed a defined as “an individual’s dispositional incapac-
ity to endure the aversive response triggered by cated by the social context of threat that emerges
the perceived absence of salient, key, or sufficient during times of terrorism (Comer & Kendall,
information, and sustained by the associated per- 2007).
ception of uncertainty” (Carleton, 2016, p. 31). Obsessions and worry are also frequently con-
Research has demonstrated a strong relationship fused/conflated with rumination. Rumination,
between IU and GAD in youth (Read et al., 2013; with reference to its role in depression, has been
Donovan et al., 2016), and some evidence exists defined as “repetitively focusing on the fact that
for the association between IU and OCD (Wright one is depressed; on one’s symptoms of depres-
et al., 2016). Although IU does not appear to dif- sion; and on the causes, meanings and conse-
ferentiate between OCD and GAD, it may be quences of depressive symptoms”
useful in distinguishing the two disorders from (Nolen-Hoeksema, 1991). Worry and rumination
others. Further research is needed to examine the are two forms of the transdiagnostic construct of
utility of IU in youth for differentiating among repetitive negative thinking differentiated in tem-
the anxiety disorders (Kendall et al., 2020). poral orientation, such that worry is more future-
oriented, whereas rumination is past-oriented
(McEvoy et al., 2013). These distinctions
Recurrent Thoughts between worry and rumination have been repli-
cated in adolescent samples (e.g., Hong, 2007;
The fact that there is a similar presentation of Muris et al., 2004). Complicating matters, fea-
recurrent, intrusive thoughts among GAD, OCD, tures of rumination may play etiological and
and PTSD (and other psychopathology) is per- maintenance roles in versions of anxiety. For
haps one of the most challenging aspects of dif- example, the compulsion to ruminate and repeat-
ferential diagnosis. Research and theoretical edly ask questions such as “why” and “what if”
discussions have emphasized the similarities of has been associated with the onset and mainte-
intrusive cognition for youth with GAD and OCD nance of PTSD (Michael et al., 2007) and can be
(Comer et al., 2004) and youth with OCD and a part of GAD (reassurance seeking) in youth.
PTSD (Huppert et al., 2005). Although there is a meaningful overlap among
Turner et al. (1992) suggest that worries and the various forms of recurrent thoughts, some
obsessions present similarly regarding presence, cognitive features may help to differentiate
form, and content within both clinical and non- between them. One distinction is the content of
clinical adults. Furthermore, worries and obses- recurrent thought. As described by DSM-5, wor-
sions are often experienced as frequent, ries characteristic of GAD consist of everyday
uncontrollable, and facilitate negative mood and life events or activities, such as health, relation-
attention biases in these groups. However, wor- ships, school, and finances. In contrast, obses-
ries and obsessions have a vulnerability factor sions tend to be more irrational and bizarre (less
distinguishing between clinical and nonclinical logically connected), although children may lack
adults. Given the overlap, some have suggested this insight (Krebs & Heyman, 2015). The con-
that obsession and worry may coexist on a single tent of obsessions tend to fall into more circum-
continuum (Langlois et al., 2000b). Huppert et al. scribed areas, including dirt/contamination, sex,
(2005) demonstrated that items on rating scales, aggression, self-doubt, and order. Children’s
such as “unpleasant thoughts come into my mind worries seem to be more logical, whereas obses-
against my will and I cannot get rid of them” and sions have an illogical (disconnected) quality
“I find it difficult to control my own thoughts,” (Comer et al., 2004). The content of recurrent
are characteristic of both OCD and PTSD. It is thoughts present in PTSD is typically associated
not surprising, and it is understandable that clini- with re-experiencing the trauma. However, such
cians and researchers find it difficult to capture cognition is not limited to the recollection of the
the exact nature of an adult’s or child’s cognitive trauma per se and may also include themes of
intrusions. This effort may be further compli- danger, negative self-schema, and evaluation of
the meaning of the trauma (De Silva & Marks, depression, and certain psychotic disorders
1999). (Starcevic & Berle, 2006). Studies support the
Distinctions have also been made regarding presence of thought-action fusion in youth with
the evaluation of the thought content. In particu- OCD (Farrell & Barrett, 2006; Libby et al. 2004);
lar, content of obsessions tends to be experienced however, one study did not find a significant dis-
as contradictory to one’s own beliefs and values, tinction in thought-action fusion between youth
whereas worries tend to be experienced as con- with OCD and youth with anxiety disorders
sistent (Langlois et al., 2000a, b; Turner et al., (Barrett & Healy, 2003). According to one study,
1992; Brakoulias & Starcevic, 2011). Given the thought-action fusion plays a minor role in anxi-
contradictory nature of some obsessions, they ety disorders but may have a particular associa-
may be accompanied by feelings of responsibil- tion with OCD, as evidenced by significantly
ity for having the thoughts (Langlois et al., 2000a; higher thought-action fusion scores in youth with
Salkovskis, 1985). However, this distinction may OCD than youth with anxiety disorders who in
vary by the content area of the obsessions (Wells turn has higher scores than non-clinical youth
& Papageorgiou, 1998). (Libby et al., 2004). Attention should be paid to
The presence or absence of identifiable trig- the interaction between thought content and
gers may help to distinguish between different meta-cognitive processes. The presence and
forms of recurrent thought, although as with quality of recurrent thoughts should be consid-
other phenomena should not be considered in ered within the full constellation of symptoms.
isolation. Studies have found that adults with
intrusive worries are more aware of specific
external or internal precipitants of the recurrent Intrusive Images
thoughts as compared to adults with intrusive
obsessions (Langlois et al., 2000a; Turner et al., The symptom presentation of both OCD and
1992), although research in youth is needed. A PTSD may include intrusive images. Intrusive
key feature of PTSD is the psychological and images associated with PTSD are typically
physiological distress in response to triggers related to the initial trauma and are frequently
associated with the trauma, which are often fragmented sensory memories (Ehlers et al.,
avoided. However, individuals with PTSD are 2004; Lafleur et al., 2011). Youth with PTSD do
frequently unaware of the triggers that give rise not engage in compulsions in response to intru-
to intrusive memories (Ehlers et al., 2004). These sive images (Lafleur et al., 2011). However,
triggers may only be loosely associated with the recent research has demonstrated that previous
trauma and may not be directly meaningful to the history of traumatic experiences may increase the
individual. presence of intrusive obsessions that may overlap
Thought-action fusion is a meta-cognitive with OCD symptoms (Barzilay et al., 2019).
construct that may help differentiate between While images in OCD are typically characterized
OCD and other disorders. This construct consists as bizarre or irrational, individuals with OCD can
of (1) believing that the presence of a thought also experience intrusive images associated with
increases the probability of an event actually a prior adverse event (De Silva & Marks, 2001;
occurring and (2) that the presence of a thought Lipinski & Pope, 1994; Speckens et al., 2007).
that is inconsistent with one’s beliefs is equiva- In OCD, sexual or violent intrusive images
lent to actually carrying out the thought (Shafran may be the most distressing or stigmatizing,
et al., 1996). Higher thought-action fusion was despite their frequent occurrence in nonclinical
found in adults with obsessive thinking than in populations (Cole & Warman, 2019). Regarding
adults with pathological worry (Coles et al., the distinction between OCD and GAD, studies
2001). It has also been suggested that thought- suggest that obsessions more frequently occur in
action fusion may play an etiological and main- the form of intrusive visual images than do wor-
taining role in additional disorders, such as GAD, ries (Gillet et al., 2018). Pathological worry typi-
cally takes the form of verbal cognition rather increases with age, suggesting that children may
than visual images and has been described as a be better able to identify their physiological
“chain of thoughts” (Borkovec et al., 1983). In symptoms associated with anxiety as they mature
contrast, intrusive images are characterized as (Crawley et al., 2014; Ginsburg et al., 2006;
brief mental flashes that are shorter in duration Choudhury et al., 2003).
(Langlois et al., 2000a). Among youth with anxiety disorders, those
endorsing somatic symptoms have been found to
have more severe psychopathology compared to
Physical Symptoms those with anxiety disorders who do not endorse
somatic symptoms. This finding includes more
Somatic symptoms are commonly experienced severe anxiety, poorer global functioning, poorer
by youth with anxiety disorders and have been academic performance, and higher rates of school
associated with anxiety severity and impairment refusal (Ginsburg et al., 2006; Storch et al.,
(Ginsburg et al., 2006; Storch et al., 2008a, b). In 2008a, b; Last, 1991; Hughes et al., 2008).
a sample of anxiety-disordered youth, over 95% Although evidence of somatic complaints is
endorsed at least one somatic symptom (Crawley not required for a diagnosis of OCD, physical
et al., 2014). Children with anxiety frequently symptoms are common among youth with this
report headaches, stomachaches, muscle tension, disorder. The most frequently experienced physi-
sweating, drowsiness, and jittery feelings (e.g., cal symptoms include tension and restlessness
Crawley et al., 2014; Eisen & Engler, 1995; Last, (Storch et al., 2008a). Storch et al. (2008b) found
1991). that sleep-related difficulties were associated
The substantial overlap among the physical with anxiety severity in children with OCD and
symptoms associated with the various anxiety may be relatively common among these youth.
disorders in youth makes it difficult to determine Children with OCD and hoarding symptoms have
a diagnosis based on this factor alone. Studies been found to exhibit higher levels of somatic
examining the relationship between anxiety dis- complaints relative to non-hoarders with OCD,
order diagnosis type and somatic symptoms have suggesting that physical symptoms may vary
found mixed results. Crawley et al. (2014) found within OCD (Storch et al., 2007). The role of
that youth with GAD and SAD reported more physical symptoms in OCD is particularly
frequent and severe somatic symptoms than nuanced as somatic concerns also characterize
youth with social anxiety disorder, which may be the nature of some children’s obsessions and/or
due to diagnostic criteria of somatic symptoms compulsions (Ivarsson & Valderhaug, 2006).
DSM IV for GAD and SAD rather than social Thus, it may be difficult to differentiate between
anxiety. Hofflich et al. (2006) found that children a child’s actual experience of somatic complaints
with GAD, social anxiety, and separation anxiety and preoccupation with such concerns. Gathering
disorder did not differ in the frequency with detailed information regarding children’s true
which they reported somatic symptoms or with physical symptoms, beliefs about bodily sensa-
regards to the presence of any specific somatic tions, and mental/behavioral responses may aid
symptom. Interestingly, children with a principal clinicians in distinguishing OCD from other anx-
diagnosis of GAD reported a wider variety of iety disorders.
physical symptoms than those listed in DSM-5, Somatic symptoms appear to be a common
(i.e., shaky and jittery, having chest pain, feeling reaction to trauma in children (Bailey et al., 2005;
strange, weird or unreal, heart racing or skipping Escobar et al., 1992; Gobble et al., 2004) and
beats, and feeling sick to their stomach). Given warrant specific attention as they are associated
the lack of significant group differences across with negative social, emotional, and academic
anxiety disorders, these somatic complaints may outcomes (Campo et al., 1999). In particular,
not be specific to GAD. The number of somatic symptoms can include physical reactivity and
complaints reported by children with GAD symptoms that are similar to those experienced
during the traumatic event. (APA, 2013). A study what is being avoided (e.g., an object, a situation,
of PTSD symptoms among children in the New an image), and the function of the avoidance,
Orleans area following Hurricane Katrina found when the avoidance takes place and what, if any,
headaches, nausea, and upset stomach to be the circumstances facilitate coping. Answers to these
most commonly reported somatic symptoms questions inform an accurate diagnosis and effec-
(Hensley & Varela, 2008). Consistent with the tive treatment and can help differentiate between
earlier discussion of anxiety sensitivity in PTSD, OCD, PTSD, and GAD.
children in the study with high anxiety sensitivity Research suggests that worry may act as the
and high trait anxiety may have had a higher risk avoidance mechanism in GAD. Worry has been
of developing PTSD and somatic symptoms fol- defined as an attempt at problem-solving to pre-
lowing exposure to the traumatic event. Knowing vent the occurrence of negative outcomes
whether children possess these characteristics (Borkovec et al., 1983). Children and adolescents
may help identify youth who are most likely to with GAD may specifically engage in cognitive
develop trauma reactions, which can in turn aid avoidance techniques by means of thought sup-
with diagnosis and intervention. pression, distraction, and thought substitution to
Garnering contextual information surround- decrease the intensity of worries (Hearn et al.,
ing the onset of physical symptoms is likely to be 2017), and parents may facilitate and maintain
more useful in determining a diagnosis than this avoidance through over-controlling their
solely assessing the presence of a particular child’s environment and decreasing response to
somatic complaint. If physical symptoms are the exposure situations (Aktar et al., 2017). Overall,
primary presenting problem, it is necessary to the evidence supports the “avoidance theory of
examine the context in which these symptoms worry” (Borkovec et al., 2004), suggesting that a
occur. When a child reports a physical symptom, primary function of worry in GAD is to enable
it can merit parental attention – more attention individuals to avoid negative outcomes, negative
than would be assigned if the child only felt emo- bodily feelings, as well as other even more dis-
tionally unsettled. Indeed, the functional impact tressing thoughts. Of interest, this notion has
of a child’s reporting physical complaints (stay applicability to the parents of anxious youth
home from school, receive care) may unwittingly (Tiwari et al., 2008).
buttress such reports. Individuals with OCD engage in a wide range
of compulsions that are believed to deactivate
and avoid threatening images, thoughts, or out-
Avoidance comes. According to Salkovskis (1985, 1989),
this behavior stems from a person’s inaccurate
Avoidance is central but not unique to GAD, belief that they have control over whether such
OCD, and PTSD. Avoidance is characteristic of outcomes will occur (recall thought-action
the anxiety disorders generally and may be pres- fusion). The implied responsibility that comes
ent in other forms of psychopathology. Avoidance with this way of thinking translates into a pattern
refers to making a response that the individual of behavioral neutralizing responses which reflect
thinks/believes is necessary to prevent a negative attempts to escape or avoid the feared outcome
condition, despite the response being unneces- (Salkovskis, 1996). These avoidance-focused
sary. Individuals with an anxiety disorder tend to efforts include compulsions that are consistent
avoid an event, outcome, or thought which is with the associated fear (i.e., repetitive hand
greatly feared and may engage in avoidance washing to avoid catching germs) as well as those
when the outcome of the feared situation or event that lack a rational connection (i.e., touching
is unknown or ambivalent (Palitz et al., 2019). objects in a symmetrical fashion to prevent harm
Individuals use avoidance to minimize or obviate from befalling a loved one). Additionally, inter-
the potential for a negative outcome. Clinicians nal avoidance may be present in the form of men-
should determine the details of the avoidance, tal rituals such as repetitively thinking about a
word or phrase until the interfering discomfort toms warrants comprehensive assessment to rule
has been alleviated. Parents may facilitate youth’s out the presence of OCD.
maintenance of compulsions, aiding youth in rit-
ualistic behaviors to avoid feared outcomes (e.g.,
reducing demands to allow time for compulsions; Reliability and Validity of Diagnosis
Stewart et al., 2017) and through accommoda-
tions of the avoidance (Kagan et al., 2018). GAD typically presents first in school-aged chil-
Cognitive processes present in adults with OCD dren and is characterized by excessive worries
that have been linked to compulsions, such as that a child finds difficult to control. The course
appraisals of responsibility, have been found to of anxiety symptoms can follow many different
exist in children with OCD as well. However, patterns through development, with GAD and
many of these processes were not found to distin- social anxiety disorder being the most persistent
guish between youth with OCD and youth with (Voltas et al., 2017), and some anxiety symptoms
other anxiety disorders (Barrett & Healy, 2003). having links to later mood disorders (Cummings
Such findings provide further evidence of the et al., 2014). In a follow-up study of youth
considerable diagnostic overlap among anxiety- patients treated for an anxiety disorder through
related disorders. Although there are several either cognitive-behavioral therapy, a selective
overlapping features of anxiety disorders, serotonin reuptake inhibitor, their combination,
research does indicate that compulsions are typi- or placebo, 30% were chronically ill, and 48%
cally unique to OCD and flashback-related avoid- had relapsed (Ginsburg et al., 2018). Additionally,
ance is typically unique to PTSD (Goodwin, youth with GAD are frequently diagnosed with a
2015). second anxiety disorder, as well as other disor-
Youth with PTSD may engage in avoidance ders such as attention deficit hyperactivity disor-
with the express purpose of distancing them- der (ADHD), oppositional defiant disorder
selves from stimuli associated with the trauma. (ODD), and depression (Kendall et al., 2001;
During a traumatic event, a strong association is Walkup et al., 2008).
formed with corresponding contextual cues When assessing for GAD in youth, clinicians
which then come to signal the presence of danger typically obtain information from adults such as
(APA, 2013; Runyon et al., 2013). This associa- parents and teachers and should pay attention to
tion leads youth to avoiding places, people, and behavior changes and physical complaints (e.g.,
activities that trigger painful memories. In addi- upset stomach, sleeping patterns, school avoid-
tion to being directed at external triggers, avoidance). When assessing among adolescents, clini-
ance in PTSD can also be directed at internal cians can rely more on the patient’s report
experiences. Youth with PTSD will often make a (Panganiban et al., 2019). Measures that are con-
concerted effort to avoid thoughts and feelings sidered validated screening tools for GAD (see
that might remind them of the immense distress also Creswell et al., 2020; Fleischer et al., 2020)
they previously experienced, including hyper- in youth include the Screen for Childhood
arousal symptoms (e.g., increased heart rate, etc.; Anxiety Related Emotional Disorders (SCARED;
Runyon et al., 2013). Research demonstrates that Birmaher et al., 1999), the Multidimensional
avoidance in individuals with PTSD may further Anxiety Scale for Children (MASC; March et al.,
generalize to aversive situations not related to 1997; Villabø et al., 2012), and the Spence
their trauma experience (Sheynin et al., 2018). Children’s Anxiety Scale (SCAS; Spence, 1998).
Compulsive urges can strictly occur within the Approximately half of all OCD cases have
context of PTSD (i.e., compulsion of thinking their onset in childhood and adolescence
“good thoughts to cancel out images of a dying (Janowitz et al., 2009). OCD that begins in child-
friend”; De Silva & Marks, 2001, p. 173) and are hood, and goes untreated, frequently persists into
not necessarily indicative of a comorbid diagno- adulthood, with one meta-analysis finding that of
sis of OCD. However, the presence of such symp- children and adolescents diagnosed with OCD,
60% had either full, or subthreshold OCD symp- degree of commonality that makes differential
toms persist (Stewart et al., 2004). Without ade- diagnosis a challenge. Consideration of this issue
quate treatment, the majority of patients begs the question of whether the disorders under
experience symptoms with a chronic and fluctu- examination truly reflect distinct entities, each
ating course. with their own unique etiology and underpin-
Comorbid diagnoses are especially common nings, or whether these disorders are better con-
in OCD in youth and include but are not limited ceptualized using a unified construct with varying
to depression, social anxiety, and substance use manifestations. Speaking to this question, symp-
(Douglass et al., 1995). High rates of comorbidi- toms of GAD, PTSD, and OCD are typically not
ties can make differential diagnoses particularly specific to one particular disorder. Treatment
challenging. To assess for OCD in youth, scales strategies that emerge from a cognitive-behavioral
that are considered to have acceptable psycho- framework (Kendall, Suveg, & Kingery, 2006),
metrics include the Children’s Yale-Brown- though applied with some variations for the spe-
Obsessive-Compulsive Scale (CY-BOCS; cific disorders, are similar and consistent and
Goodman et al., 1991) and the Obsessive- have been found to be effective for several of the
Compulsive Inventory – Child Version (OCI-CV; emotional disorders in youth (see Ollendick &
Foa et al., 2010). King, 1998).
Epidemiologic studies have found high rates Additionally, although genetics are not the
of childhood and adolescent exposure to trau- focus of this review, there are data suggesting
matic events, but only about 16% of youth that the genes for anxiety disorders may be
exposed to a traumatic event develop PTSD shared, as opposed to distinct (Hudson & Rapee,
(Alisic et al., 2014). Approximately one-third of 2004; Levey et al., 2020), and that similar changes
youth with PTSD experience a chronic course in the brain occur in several anxiety disorders
that lasts several years (McLaughlin et al., 2013). (see Sinha, Mohlman, & Gorman, 2004). As
When assessing for PTSD in youth, one must advances in the field (e.g., genetics, neuropsy-
determine whether the symptoms follow and are chology, cognition, behavior, emotion) provide
due to exposure to a traumatic event, rather than findings, a reconceptualization of anxiety, or sev-
a different psychological disorder. Childhood eral types of anxiety, may be reconsidered as one
trauma exposure and PTSD often present with disorder. This potential reconceptualization has
frequent comorbidity, particularly anxiety disor- important implications for how anxiety disorders
ders, depression, externalizing problems, self- are studied and treated.
harm, and substance use disorders (McLaughlin Overall, anxiety, OCD, and PTSD may be bet-
et al., 2013). New to the DSM-5, among children ter viewed as dimensional, rather than categori-
under the age of 6, a lower threshold of symp- cal. Individuals with the highest levels of
toms is needed to diagnose PTSD. Measures with symptoms often move in and out of meeting cri-
acceptable psychometrics for assessing PTSD in teria for an anxiety disorders overtime (Caspi &
children and adolescents include the UCLA Moffitt, 2018). Further, it may be difficult to dis-
PTSD Reaction Index for Children and tinguish between developmentally appropriate
Adolescents (PTSD-RI; Steinberg et al., 2013) anxiety and pathological anxiety (Costello &
and the Clinician-Administered PTSD Scale for Angold, 1995; Pine, 1997), or anxiety that is jus-
Children and Adolescents (CAPS-CA; Nader tified by current environmental circumstances
et al., 1996). (covid19). Although one or two symptoms may
distinguish between persons with or without a
diagnosis according to DSM-5 classification, in
Implications actuality these individuals may nevertheless look
quite similar to their nondiagnosed counterparts.
The essential features of GAD, OCD, and PTSD, In a study of European adolescents, subthreshold
as currently defined by DSM-5, have substantial anxiety was associated with increased suicidality
and functional impairment (Balazs et al., 2013). intrusive images, physical symptoms, and avoid-
Since the inception of DSM, the number of child- ance. Further, mention was made of recom-
hood diagnoses has expanded quite rapidly and mended screeners. Differentiating between GAD,
additional diagnoses have been suggested (Silk OCD, and PTSD requires an informed, skillful,
et al., 2000). However, before the field incorpo- and nuanced approach.
rates new diagnostic categorizations, bigger and
overarching issues surrounding classification –
categorical or dimensional approaches (Drabick, References
2009; Maser et al., 2009) – merit consideration
and research evaluation (see also Jensen et al., Aktar, E., Nikolic, M., & Bögels, S. M. (2017).
Environmental transmission of generalized anxiety
2006). A refinement of our classification scheme, disorder from parents to children: Worries, expe-
reflecting the empirical research, will likely facil- riential avoidance, and intolerance of uncertainty.
itate better understanding and care for youth with Dialogues of Clinical Neuroscience, 19(2), 137–147.
anxiety and its disorders. Alisic, E., Zalta, A. K., Van Wesel, F., Larsen, S. E.,
Hafstad, G. S., Hassanpour, K., & Smid, G. E. (2014).
As the current classification system stands, Rates of post-traumatic stress disorder in trauma-
diagnostic categorization can serve both to facili- exposed children and adolescents: Meta-analysis. The
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PTSD symptoms among trauma-exposed inpatient
Cognitive Behavioral Models
of Phobias and Pervasive Anxiety 4
Dean McKay
Over the last several decades, the expansion of anxiety (Matthews & MacIntosh, 1998). Recent
cognitive behavioral models of anxiety disorders literature supports the findings related to reaction
has led to improvements in therapeutic interven- time differences for subtle cues and has shown
tions and treatment outcomes. Behavioral models that cognitive biases have clear neurological cor-
are dependent on learning processes and condi- relates (McKay et al., 2009) and draw on atten-
tioning potentials (such as the non-associative tion resources, particularly in youth (i.e., Smith
account; Menzies & Clarke, 1995). Further, con- et al., 2021). These findings have collectively
temporary learning theories suggest that anxiety shown the robust nature of specific cognitive
serves as a conditioned response, as well as an biases in understanding the etiology and mainte-
unconditioned response, leading to future condi- nance of anxiety in general. At the same time,
tioning for anxiolytic stimuli (Bouton et al., cognitive errors that are articulated by anxious
2001; Zinbarg et al., 2022). individuals have been effective at determining
There are two major perspectives that inform a methods of intervention (see, e.g., McKay &
purely cognitive perspective on anxiety disor- Storch, 2009)
ders. On the one hand, cognitive therapy-based The aforementioned research describes com-
models have emerged that posit two central plementary perspectives on anxiety disorders that
dimensions of anxiety include an overestimation have, for the most part, been integrated into a
of danger, threat, and fear, as well as an underes- comprehensive framework constituting cognitive-
timation of one’s abilities to cope with such behavioral theory for anxiety. This line of work
threats (Beck et al., 1985). On the other hand, an has been highly influential in the development of
extensive literature describes cognitive biases treatment for anxiety for all ages. Indeed, the
based on automatic processing of environmental majority of empirically supported treatments for
stimuli (Williams et al., 1997). The former per- anxiety disorders are cognitive-behavioral in ori-
spective is predicated on the ability of individuals gin (Chambless & Ollendick, 2001).
to articulate cognitive errors that occur in Common to models of specific anxiety disor-
response to specific events, while the latter is not ders is threat appraisal in conjunction with learn-
reliant on client report, but instead on reaction ing as per the above description. Specific
time and biases evident for subtle cues related to components are introduced intended to isolate
the ways a specific disorder differs from others,
D. McKay (*) and the arrangement and constellation of compo-
Department of Psychology, Fordham University, nents that result in anxiety are also deemed
Bronx, NY, USA unique. The aim of this chapter is to critically
e-mail: mckay@fordham.edu

https://doi.org/10.1007/978-3-031-14080-8_4
46 D. McKay
Table 4.1 Common features of anxiety disorders: two access or construction involves the cognitive pro-
experimental perspectives
cess of decision-making whereby one or more
Cognitive errors Info. processing biases responses are recalled from memory or created
Overestimation of Encoding process for the situation. Finally, the individual under-
danger/threat selectively biased towards
threat goes response selection whereby responses are
Overestimation of fear Interpreting ambiguous evaluated in terms of a variety of factors, and the
information as threatening individual finally produces the selected response
Underestimation of Memory biases favoring through enactment. According to Dodge’s infor-
coping abilities recall of threatening info mation processing system model, anxiety disor-
Overactive threat/
ders are the result of dysfunctions occurring
danger schemas
during one or more of these stages.
A third model works to integrate Kendall’s
consider the degree those components of anxiety theory of childhood anxiety (Kendall & Ronan,
disorders models are unique to the disorders they 1990) with Dodge’s model of information pro-
purport to describe (see Table 4.1). cessing to highlight distortions and deficits that
occur throughout the stages of processing
(Daleiden & Vasey, 1997). Specifically, the
ognitive Models of Anxiety:
C encoding process of children with anxiety disor-
General Considerations ders may be influenced by a narrowing focus and
selective attention to threatening information.
Broadly, cognitive models for anxiety have an There is evidence for such an attention bias in
implicit basic assumption – that anxiety reactions both normal (Field, 2006) and anxious children
are “fast” responses to environmental stimuli and (Watts & Weems, 2006; Murrary et al., 2009).
may stand impervious to “slow” (i.e., more delib- Such children may also interpret ambiguous
erative) thinking (see Kahneman, 2011). Several information as threatening, make negative attri-
models have attempted to describe the cognitive butions about new information, expect negative
processes occurring in childhood anxiety disor- outcomes, and have low self-efficacy in coping
ders. One early model emphasized the role of with threatening situations. Such biases in the
schemas and cognitive deficit and distortion. encoding and interpretation stage may also lead
From this point of view, schemas related to dan- to an increased reliance on avoiding and escaping
ger and threat are believed to be overactive in threatening situations, as opposed to engaging in
children with anxiety (Kendall & Ronan, 1990). problem-focused coping. While these models
Additionally, such children also lack or are have been helpful in understanding general pro-
unable to use adaptive coping skills and suffer cesses that occur in childhood anxiety disorders,
from cognitive processes that are biased or erro- there is still much to be done in order to better
neous. Conversely, another model emphasized a understand cognitive dysfunctions that are spe-
stage-process approach whereby childhood anxi- cific to each of the anxiety disorders. Similar to
ety could be understood in the context of infor- this model, Weems and Watts (2005) posit that
mation flowing through the information childhood anxiety may be related to three cogni-
processing system (Crick & Dodge, 1994). Six tive processes: selective attention, memory
stages were identified as part of normal cognitive biases, and negative cognitive errors. In other
processing. During encoding, information can be words, children with anxiety tend to pay more
attended to for further processing, or ignored. If attention to threatening stimuli, remember threat-
attended to, information then undergoes interpre- ening information, and have more biased inter-
tation, whereby meaning is attached by the indi- pretations of events and situations as fearful or
vidual. Next, the goal clarification or construction threatening. Evidence for this latter model has
stage involves the activation or construction of a shown that selective attention, memory bias, and
new goal to meet situational demands. Response cognitive errors are correlated with childhood
4 Cognitive Behavioral Models of Phobias and Pervasive Anxiety 47
anxiety problems, but is unable to show specific cognitive models of anxiety to inform treatment
relationships between these three cognitive pro- and predict outcome. However, as will be seen
cesses and specific anxiety symptoms or disor- below, the research that has examined the content-
ders (Watts & Weems, 2006). specificity hypothesis with anxiety disorders in
In summary, contemporary cognitive models children is mixed and suggests only partial sup-
encompass elements from the original notion of port for the specificity of cognitions among dis-
cognitive errors that were articulated by Beck orders. One major difficulty in linking specific
et al. (1985) and emphasize the way information cognitions with specific anxiety disorders is the
is processed (i.e., directed attention, encoded, high degree of comorbidity found among anxiety
and recalled) in the etiology of childhood anxiety disorders (Last et al., 1987, 1992; Micco &
disorders. Modern conceptualizations emphasize Ehrenreich, 2010; O’Neil et al., 2010; see also
automatic processing in addition to errors in Chaps. 2, 3 and 13 this volume). Because of this
thinking that perpetuate anxiety responses. overlap among diagnostic categories, it is diffi-
Behavioral models associated with learning are cult to demonstrate specificity among cognitive
involved insofar as learning leads to selective content without also experiencing similar degrees
encoding of material. Nevertheless, treatment for of overlap.
childhood anxiety, regardless of specific disorder, One early study investigating the content of
emphasizes both cognitive approaches and cognitions compared the measurements of cogni-
behavioral interventions. tions in a group of depressed, anxious, and mixed
depressed-anxious fourth, fifth, sixth, and sev-
enth graders and found few differences between
Content-Specificity Hypothesis groups (Laurent & Stark, 1993). While no differ-
ences in anxious cognitions were found between
The idea that various disorders have specific and depressed, anxious, and mixed depressed-anxious
unique cognitive processes is not new and goes groups, the depressed group did endorse more
back to early cognitive models positing that anxi- depressive cognitions than the other two groups.
ety and depression are caused by specific types of While this study did not find support for specific-
cognitive dysfunctions unique to each disorder ity of cognitions among anxiety disorders, it did
and has been termed the cognitive content- lend backing to the theory that positive and nega-
specific hypothesis (Beck, 1976; Beck et al., tive affect are two-dimensional variables impor-
1985). For example, the content of cognitions tant in understanding anxiety and depression.
that gives rise to social anxiety disorder would be One small study compared the interpretations
distinctive from the content of cognitions that of ambiguous events of four anxious children
gives rise to panic disorder. Therefore, treatment with obsessive-compulsive disorder, separation
for mental disorders would involve identifying anxiety disorder, social phobia, and panic disor-
and modifying the specific cognitive distortions der, to interpretations provided by a group of
or biases that are presumed to give rise to each eight non-anxious controls and found evidence
disorder. In adults, some evidence for the content- that anxious children have a tendency to interpret
specific hypothesis has provided support for the ambiguous material as threatening (Chorpita
specificity of cognitions in identifying and treat- et al., 1996). Furthermore, when asked about how
ing various anxiety disorders (Clark, 1999; Clark they would react to the ambiguous situations,
& Fairburn, 1997; Foa et al., 1996; Stopa & anxious children tended to express plans involv-
Clark, 2000). However, a larger meta-analysis ing avoidance and assign a higher probability that
failed to find support for the content-specificity threatening events will occur. A similar study
hypothesis (Beck & Perkins, 2001). Less research investigated the cognitions of various groups of
has examined the content-specificity hypothesis children by providing them with an ambiguous
with anxiety disorders in children and suggests a situation involving either physical or social threat
need for further investigation into the ability of and then asking them to interpret the event and
48 D. McKay
say what they would do about it. When compar- in children with anxiety disorders (Hadwin et al.,
ing the cognitions of anxious children with sepa- 1997; Muris et al., 2000). While these findings
ration anxiety disorder, overanxious anxiety offer support for differences in cognitions
disorder, simple phobia, and social phobia, to a between anxiety and externalizing disorders, they
nonclinical control group, evidence for a threat still lack specificity in association with each of
interpretation bias was found within the anxious the anxiety disorders and instead point to support
group (Barrett et al., 1996). However, when com- for a general threat bias among children with any
pared to a group of oppositional defiant children, anxiety disorder.
the anxious group actually showed less threat The first study to directly investigate the
interpretation bias. Therefore, this particular cog- content-specificity hypothesis in children failed
nitive bias was useful in distinguishing anxious to find support for distinctive cognitions based
from non-anxious children, but lacked specificity upon anxiety disorder. Reactions were recorded
in distinguishing between children with opposi- from a group of children without anxiety disor-
tional defiant disorder and anxiety disorders. It is ders who were exposed to stories characterized
unknown to what extent this shortcoming can be by social anxiety, separation anxiety, or general-
attributed to methodological factors in the way ized anxiety (Muris et al., 2000). While high lev-
these studies were conducted. That is, because els of anxiety were associated with greater threat
each study grouped all anxiety disorders under perception, high ratings of threat, high levels of
one category, it is not possible to know if children negative feelings and cognitions, and an early
with different disorders provided distinctive detection of threat, no differences in cognitions
types of responses when interpreting ambiguous were found between the anxiety-specific content
information. Furthermore, for the latter study, the of the stories. However, one potential reason for
ambiguous situation involved only physical or this failure may be due to the sample’s high
social threat and may not have included enough degree of comorbidity between social anxiety,
of a variety of situations necessary to capture the separation anxiety, or generalized anxiety as
divergence of cognitions amongst anxiety measured by the Screen for Child Anxiety-
disorders. Related Emotional Disorders (SCARED), an
Yet still another study investigating the inter- anxiety assessment. Additionally, it was noted
pretations of ambiguous situations compared a that though each of the three stories were sepa-
group of children with anxiety disorders includ- rated by theme, separate sentences within stories
ing separation anxiety disorder, generalized anxi- may have included themes from other stories.
ety disorder, panic disorder, obsessive-compulsive Therefore, it is difficult to parse out the unique
disorder, social phobia, and simple phobia, to effects of each anxiety disorder on the types of
both a nonclinical control group and a group of responses provided by participants in this study.
children with externalizing disorders including Another study also attempted to identify spe-
oppositional disorder, attentional deficit and cific cognitive interpretations in children with
hyperactivity disorder, and conduct disorder social anxiety, separation anxiety, and general-
(Bogels & Zigterman, 2000). Here, it was found ized anxiety by exposing children to ambiguous
that anxious children had more negative cogni- situations and analyzing their interpretations and
tions than the externalizing group and nonclinical action plans (Bogels et al., 2003). Again, only
group; the former difference was significant, limited support was found for the content-
while the latter difference only approached sig- specificity hypothesis. Children with separation
nificance. Contrary to the findings by Barrett anxiety did report more overestimations of the
et al. (1996), it was found that the group of anx- danger of being abandoned and more underesti-
ious children also interpreted the situation as mations of their independent functioning com-
more threatening than the other two groups. pared to children with generalized anxiety
Other research has also confirmed this threat bias disorder or social anxiety. However, socially anx-
ious children reported more overestimation of (CASI; Silverman et al., 1991), the Revised
criticism and rejection and underestimation of Children’s Manifest Anxiety Scale (RCMAS;
their social competence compared to children Reynolds & Richmond, 1978), and the State Trait
with separation anxiety disorder, but not com- Anxiety Inventory for Children-Trait Version
pared to children with generalized anxiety disor- (STAIC-T; Spielberger, 1973) (Weems et al.,
der. Additionally, cognitive interpretations 2001). A measure of depression, the Children’s
associated with generalized anxiety did not differ Depression Inventory (CDI), was also included.
among the three groups. This latter finding may Again, results found support for a positive rela-
be due, again, to the high degree of comorbidity tionship between cognitive errors and child anxi-
between anxiety disorders. Similarly, children ety. Additionally, partial correlations controlling
with separation anxiety disorder and social pho- for depression indicated that catastrophizing and
bia showed a negative interpretation bias relevant overgeneralizing were related to all measures of
to their fear, though these groups could not be anxiety and that personalization was related to
distinguished from each other. Also, children most measures of anxiety. While these findings
with generalized anxiety disorder did not show lend credence to the notion that different types of
any distinguishable differences in their negative cognitive errors contribute to anxiety, it remains
interpretation bias. unknown whether or not each of the measured
As mentioned above, one study has shown categories of cognitive errors are specific to the
that selective attention, memory bias, and cogni- various anxiety disorders present in children.
tive errors are associated with anxiety symptoms Review data show that, overall, the content-
in children (Watts & Weems, 2006). Of interest to specificity hypothesis provides a useful concep-
the content-specificity hypothesis is the degree to tual framework for youth anxiety disorders (Nicol
which cognitive errors alone can account for dif- et al., 2020). However, while there have been an
ferences in the expression of anxiety symptoms. abundance of investigations, the majority employ
In the aforementioned study, cognitive errors community or unselected samples, and thus the
were measured by the Children’s Negative generalizability to clinical samples remains
Cognitive Error Questionnaire (CNCEQ), an unclear.
assessment targeting four major forms of cogni-
tive errors (catastrophizing, overgeneralization,
personalizing, and selective abstraction). pecific Disorders: Posttraumatic
S
However, measures that were used to assess anxi- Stress, Obsessive-Compulsive,
ety, the Revised Child Anxiety and Depression and Generalized Anxiety Disorders
scales (RCADS) and its parent version
(RCADS-P; Chorpita et al., 2000), assessed for a Posttraumatic stress disorder (PTSD) has been
range of anxious and depressive symptoms to found in both adults and children, although until
produce an overall score and were not able to recently most research on cognitive models of
provide information about specific diagnosis. PTSD has been focused on adults. More recently,
While scores on these anxiety measures were sig- cognitive models of adult PTSD have been
nificantly and positively correlated with the applied to working with children with this disor-
CNCEW total and subscale scores, it was not der (Vickers, 2009). An adult model proposed by
possible to investigate whether particular anxiety Ehlers and Clark (2000) was applied to under-
disorders were associated with unique types of standing the presentation and treatment of two
cognitive errors as assessed by the CNCEQ. An children with PTSD. This model views PTSD as
earlier study also investigated the relationship a paradoxical disorder characterized by intense
between specific cognitive errors as measured by fear of a future threat propagated by a severely
the CNCEQ and measures of anxiety as mea- terrifying event that happened in the past.
sured by the Childhood Anxiety Sensitivity Index Because this event has been processed in a way
50 D. McKay
that the threat of danger remains current, indi- ing in worry process (Davey & Levy, 1998) and
viduals with PTSD are observed to engage in a its interfering role in information processing
variety of avoidance behaviors that are ineffec- (McKay, 2005). However, this does not suggest
tive at reducing threat. This model of PTSD specificity of catastrophizing or worry to GAD.
views cognitions and the personal meaning of the Indeed, it may not necessarily be the case that
terrifying event as a core process, rather than these cognitive processes are specific. Recent
simply emphasizing conditioning as earlier mod- treatment trials targeting worry, and associated
els of PTSD have done. The two cases presented cognitive processes, have shown positive out-
by Vickers (2009), along with several other stud- come in children with GAD as well as those with
ies applying the Ehlers and Clark model, have separation anxiety and social anxiety (Kendall
offered some promising though limited support et al., 2008; Suveg et al., 2009).
for using an adult model of cognitive processes in
explaining a childhood anxiety disorder (Stallard,
2003; Ehlers et al., 2003). Selective Mutism
Obsessive-compulsive disorder (OCD) is
another disorder that presents in both adults in Current conceptualizations of selective mutism
children. While there has been evidence to sup- (SM) suggest two major types: anxious and/or
port the specificity of cognitions associated with oppositional. For the present purposes, we will
OCD in adults (e.g., Salkovskis et al., 2000; Frost restrict our focus to the anxious type, which has
& Skeketee, 1997), less research has been con- been considered similar to social anxiety (Beidel
ducted to determine whether or not similar cogni- & Turner, 2007; Freeman et al., 2004). One factor
tions occur in childhood OCD. One study that did that has been considered a significant contributor
focus on children investigated whether cogni- to selective mutism in relation to children is
tions found in adult OCD were also found in behavioral inhibition (Beidel & Turner, 2007), a
childhood OCD, including inflated responsibil- temperament that is present from a very early
ity, overimportance of thoughts, and perfection- age. However, the research has generally sug-
ism (Libby et al., 2004). Results showed that gested that behavioral inhibition is a risk factor
children with OCD displayed higher levels of for a wide range of anxiety disorders and is not
inflated responsibility as compared to a group of specific to SM (summarized in Lonigan &
children with other anxiety disorders and a non- Phillips, 2001). There have not been any investi-
clinical control group. Results also showed a gations evaluating cognitive factors contributing
higher level of thought-action fusion, the belief to SM.
that one’s thoughts can have direct effects on the
environment, in children with OCD as compared
to children with other anxiety disorders and a Separation Anxiety Disorder
nonclinical control group. Moreover, while per-
fectionism was not found to be uniquely associ- As noted above regarding GAD, treatment of sev-
ated with childhood OCD, a subscale of the eral common factors associated with anxiety gen-
perfectionism measure, concern over mistakes, erally appears to confer a benefit on children
was significantly related to children with OCD as suffering from separation anxiety (i.e., Kendall
compared to children in the other two groups. et al., 2008). With respect to separation anxiety
Finally, generalized anxiety disorder (GAD) is disorder (SAD) specifically, several factors have
a disorder present across age ranges. Most mod- been implicated in the etiology and maintenance
els of GAD emphasize the role of worry control of the disorder. Among these are anxious attach-
and catastrophizing in the etiology and mainte- ment style, parental anxiety, and comorbid psy-
nance of the disorder (Borkovec et al., 2004). chiatric conditions (summarized in van Dyke
Some research supports the role of catastrophiz- et al., 2009). However, these do not represent a
comprehensive model of the disorder’s unique This leads to an important distinction that has
characteristics. Nevertheless, treatment relying been drawn in recent years regarding the role of
on general cognitive behavioral principles such behavioral interventions in cognitive therapy
as coping skills, anxiety management, and expo- (i.e., behavioral experiments) versus exposure
sure has collectively led to significant per se. Some have argued the behavioral experi-
improvement (Kendall et al., 2008; Suveg et al., ments allow therapists to access cognitions that
2009; Walkup et al., 2008). are either unique to the individual or to the dis-
order in question (i.e., Bennett-Levy et al.,
2004). Alternatively, it has been argued that
pecificity of Treatment for Unique
S behavioral experiments provide a mechanism,
Cognitive Features of Anxiety through exposure, to provide corrective feed-
Disorders back that alters cognitive processes indirectly
(McMillan & Lee, in press). This would suggest
From the available literature, it appears that treat- that a typology of environmental cues could be
ment for childhood anxiety disorders using developed that would serve a similar diagnostic
cognitive-behavior therapy is highly efficacious. value to the current Diagnostic and Statistical
Indeed, meta-analytic reviews have shown large Manual. The prospect of a behavioral typology
effect sizes associated with treatment that would lead directly to specific interventions
(Abramowitz et al., 2005; Bear et al., 2020; has been entertained in the past (Kanfer &
Silverman et al., 2008). Bear et al. (2020) showed Saslow, 1969). These have not lead to system-
that treatment employing specialty treatment atic diagnostic schemes, but point to the possi-
shows large effect sizes when compared to bility that models should be developed with
treatment-as-usual (TAU), although it is noted specificity in mind.
that TAU is highly variable. This is encouraging
since anxiety disorders are associated with sig-
nificant disability and can impair academic and Conclusion
social functioning in lasting ways.
While the news is encouraging, it has become In conclusion, the evidence supporting a
increasingly important that specific mechanisms content-specificity hypothesis for anxiety disor-
associated with the development of disorders be ders remains mixed and in need of further
clearly articulated in order to advance our under- review. While there is strong evidence that cog-
standing of how to prevent specific psychological nitive errors are associated with anxiety and
problems, as well as to improve the efficiency of depression in general, the degree to which par-
current interventions. What this review has shown ticular disorders map onto specific cognitive
is that whereas treatment as currently conceived errors is still unknown. Such a mapping is
is effective, there are few unique cognitive or important in bolstering a cognitive model of
behavioral factors tied to individual anxiety dis- anxiety disorders in children, as well as adults,
orders (see Tables 4.2 and 4.3). Cognitive vari- because it clearly identifies the mechanism
ables such as coping or proneness to involved in the development of an anxiety disor-
catastrophizing are instead more likely to be der in an individual. Without such knowledge,
components evident across anxiety disorders, and current cognitive models remain muddled and
the alleviation of these features produces a gen- vague, limiting themselves to only pointing at
eral therapeutic benefit. Insofar as there are spe- general patterns rather than the more detailed
cific behavioral manifestations, it appears that cognitive processing involved in etiology and
directly targeting these using behavioral inter- maintenance of anxiety that one would desire in
ventions alone is also efficacious. treatment.
52 D. McKay
Table 4.2 Content specificity in anxiety disorders

Disorder Unique components References
Separation anxiety Overestimation of the danger of being abandonded Bogels et al. (2003)
disorder Underestimation of independence van Dyke et al.
Anxious attachment style (2009)
Parental anxiety
Comorbid psychiatric conditions
Social anxiety disorder Overestimation of criticism and rejection Bogels et al. (2003)
Underestimation of social competence
Selective mutism Behavioral inhibition Beidel and Turner
(2007)
Posttraumatic stress Intense fear of a future threat due to manner of processing of Ehlers and Clark
disorder prior threatening event (2000)
Obsessive-compulsive Inflated responsibility Libby et al. (2004)
disorder Overimportance of thoughts
Perfectionism
Table 4.3 Mixed or limited support for specificity of Beidel, D. C., & Turner, S. M. (2007). Shy children, pho-
hypothesized cognitive content bic adults: nature and treatment of social anxiety dis-
order (2nd ed.). American Psychological Association.
Generalized anxiety disorder
Bennett-Levy, J., Butler, G., Fennell, M., Hackmann, A.,
Anxiety disorders in general Mueller, M., & Westbrook, D. (2004). Oxford guide to
Anxiety disorders vs. depressive disorders behavioural experiments in cognitive therapy. Oxford
Anxiety disorders vs. oppositional defiant disorder/ University Press.
conduct disorder Bogels, S. M., & Zigterman, D. (2000). Dysfunctional
Phobia cognitions in children with social phobia, separa-
Panic disorder tion anxiety disorder, and generalized anxiety dis-
order. Journal of Abnormal Child Psychology, 28,
Note: This list is derived from research examining content
205–211.
specificity either among disorders or between disorders in
Bogels, S. M., Snieder, N., & Kindt, M. (2003). Specificity
children
of dysfunctional thinking in children with symptoms
of social anxiety, separation anxiety, and generalized
anxiety. Behaviour Change, 20, 160–169.
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Neurochemistry of Childhood
Anxiety Disorders 5
Lauren Havel, Pranav Mehta, Ankit Gautam,
Edward Danielyan, and Kirti Saxena
Overview of Neurochemistry its dendrite and down the axon until it reaches the
and Neurotransmission nerve terminal. Subsequently, the plasma mem-
brane depolarizes which increases the entrance of
Neurochemistry describes the molecular basis of calcium ions through voltage-sensitive calcium
both the function and dysfunction of nervous sys- channels. As a result, a series of proteins are acti-
tem tissues. In studying the neurochemical basis vated, allowing vesicles to fuse with the preter-
for psychiatric disorders, a significant focus is on minal membrane and release its transmitter
neurotransmission, the transfer of impulses content into the synaptic cleft. Afterward, the
between neurons or between neurons and effector transmitter can bind with its receptor on the post-
cells. Neurotransmission occurs through chemi- synaptic neuron (Theibert, 2020).
cal substances known as neurotransmitters at the Neurotransmitters may be excitatory or inhibi-
synapse. There are several different types of neu- tory based on the characteristics of their receptor,
rotransmitters, including amino acids, peptides, and many neurotransmitters can interact with
monoamines, and more. Molecules such as neu- multiple receptor types or subtypes. Transmitter
rotrophic factors, steroid hormones, and small amino acids and amines are often transported
organic molecules also play important roles in from the synaptic cleft into nerve terminals and
neuronal signaling. In neurotransmission, when glial cells via plasma membrane transporters
the receptor of a neuron receives a signal, the sig- such as the serotonin transporter. This type of
nal is transferred as an electrical impulse through transport is dependent on the sodium-potassium
ATP pump, which maintains an ion gradient
L. Havel (*) · K. Saxena essential for the transmission of electrical signals
Menninger Department of Psychiatry and Behavioral in the neuron (Siegel & Sapru, 2011).
Sciences, Baylor College of Medicine, Houston, TX, This chapter will explore the neurochemical
USA underpinnings of anxiety disorders and obsessive-
Department of Psychiatry, Texas Children’s Hospital, compulsive disorder. First, a general overview of
Houston, TX, USA neuroanatomy and neurotransmitters implicated
e-mail: Lauren.Havel@bcm.edu
in anxiety disorders will be presented. Then, the
P. Mehta anxiety disorders will be reviewed in detail,
Rice University, Houston, TX, USA
focusing on alterations in neurotransmission that
A. Gautam may influence the onset, presentation, treatment,
Government Medical College, Amritsar, India
and life course of these disorders. In this chapter,
E. Danielyan generalized anxiety disorder (GAD), social pho-
University of Portland, Portland, OR, USA

https://doi.org/10.1007/978-3-031-14080-8_5
56 L. Havel et al.
bia (SP), separation anxiety disorder (SepAD), These disruptions can stem from decreased
specific phobia, panic disorder (PD), and inhibitory signaling or increased excitatory trans-
obsessive-compulsive disorder (OCD) will be mission. Understanding the interconnectivity
discussed. between neurotransmitters across brain regions is
vital towards understanding the functional differ-
ences between various anxiety-related disorders.
Neurochemistry of Anxiety This section reviews several neurotransmitters
associated with anxiety (Martin et al., 2010).
Overview
Norepinephrine Norepinephrine (NE) is syn-
Anxiety disorders are a group of psychiatric thesized centrally in the locus coeruleus (LC).
diagnoses that share features of excessive fear There are three main groups of adrenergic recep-
and anxiety, along with related behavioral distur- tors (a1, a2, b), among which a2 post-synaptic
bances. Anxiety can be thought of as the anticipa- receptors are most commonly associated with
tion of a potential threat, while fear is the reaction depression and anxiety. a2 adrenergic receptors
to an imminent threat. Anxiety is a normal emo- are present on the cell bodies and terminals of NE
tional state; in order to be diagnosed with an neurons where they regulate the firing rate and
anxiety disorder, the severity or frequency of fear release of NE; stimulation of a2 receptors can
and anxiety must prove to be distressing and mal- decrease the firing rate of LC NE neurons. NE
adaptive (American Psychiatric Association, and related metabolites in urine, blood, and CSF
2013). The fear response begins with perception. have been found to be elevated in anxiety disor-
Most sensory perceptions are relayed through the ders including PD, specific phobia, social anxiety
thalamus into the sensory cortices, which are disorder, and GAD; such findings suggest that
responsible for the cognitive appraisal of a stimu- both central and peripheral NE is dysregulated in
lus as a threat. There are two exceptions to this anxiety disorders (Mathew & Parambi, 2020).
pathway: olfactory input (which may reach the
amygdala and entorhinal cortex directly) and vis-
ceral organ input (which may proceed from the Dopamine Dopamine is another catecholamine
brainstem nuclei to the locus coeruleus (LC)). neurotransmitter and a step in the pathway to the
This latter pathway is crucial in disorders with a synthesis of norepinephrine. It is released primar-
significant somatic component, such as panic dis- ily by the substantia nigra (SN) and acts on five
order (PD). From the sensory cortices, impulses subtypes of dopamine receptors, which are excit-
are relayed to relevant structures for emotional atory G-protein coupled receptors. Dopamine is
processing, such as frontal cortices, striatum, and implicated in numerous functions including
limbic and paralimbic structures (including the motor control, social behavior, and reward
amygdala), which in turn project to cortical and salience. Dopamine has not been studied exten-
subcortical “output” areas to coordinate a sively in most anxiety disorders, but given its
response to the stimulus. Alterations in neuro- important role in complex human behavior, it is
chemistry and neurotransmission at any of these increasingly becoming a target of investigation
junctures may contribute to anxiety disorders (Mathew & Parambi, 2020).
(Strawn et al., 2014).
Serotonin Mechanistically, serotonin (5-HT) is

Neurotransmitters and Anxiety synthesized from tryptophan in the raphe nuclei.
First, tryptophan is converted into
Anxiety disorders as a whole are characterized 5-
hydroxytryptophan (5-HTP) by tryptophan
by neuroendocrine, neurotransmitter, and neuro- hydroxylase, an enzyme present in serotonergic
anatomical disruptions (Stein & Steckler, 2010). neurons. Then, aromatic I-amino acid decarbox-
5 Neurochemistry of Childhood Anxiety Disorders 57
ylase (AADC) converts 5-HTP into 5-HT through Neuropeptide Y (NPY) NPY and its receptors
a calcium-dependent process. Serotonin release are involved in both anxiety and stress. NPY is
is controlled by the serotonergic soma firing rate synthesized in the arcuate nucleus, a brain region
in raphe nuclei and mediated by calcium, which which receives stress-related adrenergic input
promotes fusion of synaptic vesicles with the from the LC. Several rodent studies have sug-
plasma membrane. As we will discuss below, gested that NPY administration has anxiolytic
serotonin has been widely implicated in the and sedative effects. Likewise, NPY can antago-
pathophysiology of anxiety disorders, in part due nize CRH-induced stress responses and suppress
to early clinical findings of response to serotoner- LC firing when injected into the brainstem. As
gic medications. Polymorphisms of the 5-HT scientific understanding of the role played by
transporter (5-HTT) gene are associated with an NPY receptors (located across arcuate nucleus,
increased anxiety disorder risk, particularly when central amygdala, nucleus accumbens, septum,
coupled with stressful life events (Schiele et al., periaqueductal gray (PAG), and hippocampus)
2016). Decreased expression of 5-HTT has been improves, NPY receptor agonists may become a
associated with heightened acute anxiety goal of anxiolytic development (Mathew &
responses (Santangelo et al., 2016). The raphe Parambi, 2020).
nuclei, medial raphe, amygdala, and hypothala-
mus each interact with serotonergic aspects of
fear and anxiety through potential negative feed- Cholecystokinin Cholecystokinin (CCK) is a
back mechanisms. neuropeptide with potentially anxiogenic effects.
Key areas of the fear network are interconnected
by CCK-ergic pathways (Zwanzger et al., 2012).
Gamma-Aminobutyric Acid (GABA) GABA CCK-B receptor agonists have been reported to
is an inhibitory neurotransmitter synthesized have (1) anxiogenic effects in animals and (2)
from glutamate through the Krebs cycle. anxiogenic and panicogenic effects in both
Glutamic acid decarboxylase, the enzyme healthy and PD subjects. Suppression of CCK-B
responsible for the conversion of glutamate into receptor expression and pharmacological antago-
GABA, is encoded by the GAD65 gene. GAD65 nism can block the acquisition of a conditioned
knockout animal models are vulnerable to symp- fear response. Despite the lack of abundant suc-
toms mimicking anxiety (Müller et al., 2015). cess in clinical trials, CCK remains an attractive
Given that tonic inhibition in the amygdala is target for drug development, especially with PD
dependent on GABA, GABA and its receptors (Mathew & Parambi, 2020).
are prime neurochemical targets for understand-
ing and treating anxiety. There are two main
types of GABA receptors, one of which Substance P Substance P (Sub P) is a neuropep-
(GABA-A) is linked with anxiety; GABA-A is tide that binds to the neurokinin-1 receptor (NK-1
composed of five protein subunits surrounding a or tachykinin-1 receptor). Sub P has anxiolytic
chloride channel. Several anxiolytic compounds effects when it is injected into the cholinergic
interact with the GABA-A receptor as either allo- nucleus basalis magnocellularis. Additionally,
steric modulators or agonists, including alcohol, NK-1 activation in the hypothalamus can inhibit
benzodiazepines, and barbiturates. GABA-A the secretion of corticotropin-releasing hormone
receptors are also capable of bidirectional ago- (CRH). Antagonists of NK-1 receptors can exert
nism, a property which suggests that endogenous anxiolytic and antidepressant effects. Several
inverse agonists or endogenous agonists may NK-1 antagonists have appeared anxiolytic in
play a role in the regulation of anxiety (Mathew animal studies, and in a preliminary clinical trial,
& Parambi, 2020). the MK-869 antagonist was considered as effec-
tive as paroxetine in treating anxiety and depres-
sion (Mathew & Parambi, 2020).
58 L. Havel et al.
Generalized Anxiety Disorder inconsistent, with some studies demonstrating

increased baseline cortisol and others decreased
Generalized anxiety disorder (GAD) is a condi- or unchanged, as well as varying cortisol
tion characterized by persistent worry and anxi- responses to stressful stimuli and the dexametha-
ety about routine life circumstances such as sone suppression test (Juruena et al., 2020). One
personal health, work, and social interactions and theory advanced to explain these differences is
is associated with signs of physiologic hyper- that chronic anxiety over time blunts the HPA
arousal such as fidgetiness, muscle tension, axis response; those early in their disease course
insomnia, and appetite change (American may have increased reactivity or baseline levels,
Psychiatric Association, 2013). Patients with but over the course of the illness, HPA reactivity
GAD have been found to have dysregulation in and cortisol will decrease. Studies of hair cortisol
multiple neurotransmitter systems (Jetty et al., showing decreased long-term concentrations of
2001). cortisol in adult GAD patients (but not adoles-
Given the efficacy of SSRI medication in cents) may support this hypothesis (Kische et al.,
GAD treatment, the 5-HT system is of significant 2021; Staufenbiel et al., 2013).
interest (Maslowsky et al., 2010). Early investi- GABA is a potent anxiolytic neurotransmitter
gations of neurochemistry in all anxiety disor- at the GABA-A receptor. GAD subjects have
ders, GAD included, focused on peripheral and been found to express fewer GABA receptors in
whole-brain (via CSF sampling) neurotransmit- their frontocortical region compared to healthy
ter levels and metabolism. In the serotonin sys- subjects (Nikolaus et al., 2010). Additionally,
tem, 5-hydroxyindoleacetic acid (5-HIAA) is a female patients with GAD were found to have
marker of 5-HT turnover. Increases in urinary fewer GABA-A receptors in the L temporal pole
5-HIAA in GAD patients were reported, correlat- compared to healthy controls (Tiihonen et al.,
ing with symptom severity (Garvey et al., 1995). 1997). Peripheral studies have found decreased
However, studies of peripheral plasma concentra- expression of GABA receptor mRNA in the lym-
tions of 5-HT and 5-HIAA in GAD patients did phocytes of GAD patients, as well (Rocca et al.,
not show differences from controls (Hernández 1998).
et al., 2002). Iny and colleagues have reported Dopamine transporter activity in the striatum
finding decreases in platelet 5-HT reuptake bind- was found by Lee and colleagues to be reduced in
ing in GAD (Iny et al., 1994). Centrally, PET and GAD compared to controls (Lee et al., 2015).
SPECT studies have found no significant differ- This same study found no differences in the sero-
ence in 5-HT transporter binding density between tonin transporter in the striatum, but did not
GAD patients and healthy controls (Maron et al., investigate other areas. With regard to researched
2004b). However, there are studies indicating neurotrophic factors for GAD, one study found
associations between 5-HTT polymorphisms, that serotonin-norepinephrine reuptake inhibitor
GAD diagnosis, and response to treatment, which (SNRI) antidepressant treatments have increased
suggest dysregulation in serotonin reuptake plasma brain-derived neurotrophic factor
(Craske et al., 2017). In terms of treatment (BDNF) concentrations in GAD participants
response, effective SSRI treatment of GAD leads (Ball et al., 2013). However, there is still limited
to improved functional connectivity between the research on the association between BDNF base-
VMPFC and basolateral amygdala (Lu et al., line plasma concentration and GAD severity.
2021), suggesting improved serotonergic modu-
lation of amygdala-driven anxiety circuits
(Strawn et al., 2012). Social Phobia
The hypothalamic-pituitary-adrenal (HPA)
axis and its outflow hormone cortisol have been Social phobia (SP) is characterized by the persis-
extensively studied in GAD, given the chronic tent, irrational fear of being negatively evaluated
nature of the condition. However, results remain by others during social interactions and related
avoidance and physiologic changes (American and dopamine transporter availability correlated
Psychiatric Association, 2013). With regard to with symptom severity (Hjorth et al., 2021).
serotonergic systems, SP has been associated Dopamine D2 receptor density both within the
with increased rates of serotonin synthesis in the striatum and non-striatal areas has been found to
amygdala, raphe nuclei region, caudate nucleus, be dysregulated, although these results have not
putamen, hippocampus, and anterior cingulate been consistent (Cervenka et al., 2012; Plavén-
cortex as well as increased serotonin transporter Sigray et al., 2017).
availability in the raphe nuclei region, caudate Other neurotransmitter systems including
nucleus, putamen, thalamus, and insula cortex oxytocin and glutamate receptors are also
(Frick et al., 2015). SP is also associated with a involved with SP. In humans, oxytocin has been
decrease in autoreceptor and inhibitory 5-HT1A suggested to modulate anxiety by reducing
receptor binding sites in the amygdala and mesio- amygdala response in potentially threatening
frontal brain regions (Lanzenberger et al., 2007). social contexts (Heinrichs et al., 2009). In SP
Serotonin transporter binding potential – an indi- patients, intranasal administration of oxytocin
cator of increased reuptake activity relative to has been found to attenuate hyperactive amyg-
serotonin availability – is normalized with effec- dala reactivity to fearful stimuli (Labuschagne
tive SSRI anti-anxiety treatment in SP (Kent et al., 2010). Despite limited data on treatment
et al., 2002). outcomes, oxytocin can also improve personal
Serotonin and the HPA axis have important evaluations of appearance and speech perfor-
interactions in SP. Cortisol has been found to mance in SP subjects (Guastella et al., 2009).
increase vulnerability to and severity of SP by Regarding glutamatergic systems, SP is sug-
potentially altering the function of 5-HT1A gested to increase the ratio of glutamate to cre-
receptors in the limbic system (Lanzenberger atine in the anterior cingulate cortex (Phan et al.,
et al., 2010). Several studies have also shown that 2005). Finally, there is some evidence of inflam-
serotonin-releasing compounds such as fenflura- matory dysregulation in SP: females with SP
mine can elevate cortisol levels in SP subjects, commonly underexpress C-reactive protein and
indicating supersensitivity of the postsynaptic IL-6 (Vogelzangs et al., 2013).
serotonin receptors (Tancer et al., 1994). Other
lines of research have focused more on the
peripheral autonomic nervous system and dem- Separation Anxiety Disorder
onstrated ANS hyperactivity but not HPA hyper-
activity in socially stressful tasks in SP patients Separation anxiety disorder (SepAD) is charac-
relative to controls (Tamura et al., 2013). terized by the experience of excessive distress
Dopamine can also play an important role in when separated from home or attachment figures.
anxiety modulation, particularly in social con- Individuals with separation anxiety often worry
texts, which may activate the reward system. about the well-being or potential death of attach-
Although early studies suggested that SP subjects ment figures when separated from them. There
do not experience dopaminergic dysfunction, are two main subtypes of the disorder: childhood
more recent work has suggested otherwise. When (C-SepAD) and adult separation disorder
administered dopamine agents – sulpiride and (A-SepAD) (American Psychiatric Association,
pramipexole – Hood and colleagues (Hood et al., 2013). The research into the neurochemical basis
2010) reported that SP subjects experienced of separation anxiety disorder remains limited,
increased anxiety levels to both drugs and sug- but reveals promising directions for additional
gested the likelihood of dopamine receptor inquiry (Schiele et al., 2020).
desensitization post-SSRI treatment. Dopamine Studies of pharmacological treatment of
transporter co-expression with the serotonin SepAD with serotonergic medications (Schneier
transporter in the striatum has been found to be et al., 2017) and SepAD animal models (Spinelli
increased in SP patients compared to controls, et al., 2007) implicate the serotonin system. To
60 L. Havel et al.
date, no systematic investigation of serotonin Specific Phobia

neurotransmission has been undertaken in
SepAD. However, the endogenous opioid sys- Specific phobia is a disorder of acute fear that is
tem, often modulated by serotonin, is thought to triggered by a stimulus in the environment.
be dysregulated in SepAD (Boparai et al., 2018). Broadly speaking, there are two functional cate-
Additionally, children with SepAD may show gories of phobias. Non-experiential phobias are
increased reactivity of the HPA axis during sepa- those that occur without prior negative experi-
ration events (Brand et al., 2011). ence, such as fear of snakes in a patient without a
Attachment research suggests that oxytocin is history of snakebite. These phobias rely on evo-
crucial in establishing and maintaining close lutionarily innate, learning-independent fear cir-
caregiver attachments and is likely an important cuits, with defects in sensitization and habituation
contributor to pathological SepAD (Gottschalk & (Ipser et al., 2013). Experiential phobias rely on
Domschke, 2020). Youth with SepAD have been prior negative experiences, such as fear of dogs in
found to have decreased concentrations of sali- a person who experienced a dog attack as a child.
vary oxytocin, with direct negative associations These phobias are driven by classical condition-
between severity and oxytocin concentration ing mechanisms but are maintained long after the
(Lebowitz et al., 2016). Additionally, youth with negative experience due to deficits in extinction
SepAD had greater oxytocin responses to mater- (Garcia, 2017).
nal attachment behavior compared to other anx- Innate fear is an important component of spe-
ious youth (Lebowitz et al., 2017). Childhood cific phobia. This type of fear is highly dependent
SepAD has also been associated with variations on the amygdala (Mobbs et al., 2010); we will
in the oxytocin receptor genotype, further sup- review, in simplified terms, the neurochemical
porting its role in the pathophysiology of SepAD basis of fear regulation in the amygdala. For a
(Costa et al., 2017). more detailed outline, see Keifer and colleagues’
Adult SepAD is often studied in the context of review (Keifer et al., 2015). The amygdala, par-
other psychiatric diagnoses. The findings are ticularly the central nucleus and its extended net-
consistent with known alterations of neurochem- work, processes fear cues from a variety of inputs
istry in other anxiety disorders and further (Fox & Shackman, 2019). At rest, the fear centers
emphasize the importance of oxytocin in of the amygdala are tonically inhibited by
SepAD. Adult women’s ratings of separation gamma-aminobutyric acid (GABA), which is
anxiety were negatively correlated with levels of released locally by interneurons. Dopamine mod-
oxytocin 3-months postpartum (Eapen et al., ulates this inhibition and is released during both
2014). A-SepAD has been found to be prevalent excited and stressed states (Marowsky et al.,
in nonresponders to other anxiety disorder treat- 2005). Norepinephrine also increases fear by
ments. When those patients were treated in an reducing tonic inhibition (Onur et al., 2009).
attachment-based paradigm, Milrod and col- Serotonergic projections from the raphe nucleus,
leagues found non-significant but still drastic on the other hand, inhibit amygdala reactivity
reductions in oxytocin levels, which were associ- (Lee et al., 2013). The amygdala, in turn, projects
ated with reduced heart rate variability (Milrod to the bed nucleus of the stria terminalis (BNST)
et al., 2016). In patients with PD, major depres- (Fox & Shackman, 2019) which coordinates the
sion, and bipolar disorder, reduced peripheral behavioral and emotional responses to fear and to
platelet expression of the peripheral benzodiaze- the HPA axis which allows the body to respond to
pine receptor – commonly known as mitochon- stress.
drial translocator protein (TSPO) – has been During both anticipatory and acute fear states,
associated with the presence of SepAD (Abelli phobia patients show increased activation and
et al., 2010). Crucially, this receptor mediates the connectivity in fear circuits (Münsterkötter et al.,
rate-limiting step in the synthesis of anxiolytic 2015). It is assumed that patients with specific
neurosteroids. phobia suffer from reduced GABA-mediated
tonic inhibition of the central amygdala circuits. standpoint, as it is a valuable target for pharma-
This process is hypothesized to be mediated by cologic intervention in the treatment of specific
reduced “top-down” inhibition of the amygdala, phobia and other anxiety disorders. Extinction is
as noted by reduced ventromedial prefrontal cor- thought to be dependent on long-term potentia-
tex (vmPFC) activity in phobia patients (Hermann tion (LTP), which is mediated by glutamatergic
et al., 2009). As described above, dopamine and transmission via the NMDA receptor. Extinction
norepinephrine are both implicated in the modu- is modulated by serotonin (Amano et al., 2010)
lation of this inhibition. Beta-blockers, which and CCK (Rovira-Esteban et al., 2019). Blockade
decrease sympathetic outflow, reduce amygdala of neurotransmitters upregulated by serotonin,
reactivity (Hurlemann et al., 2010) and are useful such as GABA and the endocannabinoids, has
in treatment of specific phobias and other situa- been found to impair extinction (Marsicano et al.,
tional phobias. Serotonin is important in main- 2002). In terms of treatments, D-cycloserine is a
taining tonic inhibition in the amygdala. The partial agonist at the NMDA-R and has been
short polymorphism of the serotonin transporter found to augment extinction learning (Hofmann
gene predicts increased amygdala activation in et al., 2015). Additionally, given serotonin’s con-
response to phobic exposures (Bertolino et al., tribution to extinction, we can understand the
2005). Most studies also suggest that patients value of SSRIs in treating phobia and anxiety
have an exaggerated cortisol response during disorders.
phobic exposures (Fredrikson et al., 1985), and
treatment with cortisol blunts phobic responses
and enhances exposure therapy in treatment mod- Panic Disorder
els, suggesting a negative feedback loop (Soravia
et al., 2018). Panic disorder (PD) is a paroxysmal, often dra-
Returning to the categories of experiential vs. matic, disorder of acute physiologic and psycho-
non-experiential phobia, there are likely addi- logic fear responses. Various features of PD, in
tional neurochemical factors at play. Those with addition to its cardinal symptoms, strongly sug-
non-experiential phobia are hypothesized to be gest a neurobiological and neurochemical basis.
more vulnerable to fear sensitization and less These include high heritability, nocturnal occur-
likely to habituate to phobic stimuli. Sensitization rence, baseline autonomic hyperarousal, sensitiv-
is thought to occur via a “top-down” noradrener- ity to pharmacologic challenge, and robust
gic mechanism; repeated exposure to innately response to pharmacotherapy (Goddard, 2017).
fearful stimuli in rats leads to upregulation of NE Several neurotransmitter systems have been
receptors on the GABA-ergic amygdala interneu- implicated in panic, which taken together suggest
rons important for tonic inhibition (Rajbhandari a functional neuroanatomical and neurochemical
et al., 2016). Habituation, on the other hand, system that drives PD.
requires a reduction of “bottom-up” fear and is PD’s features consist of chronic anticipatory
associated with increased functional connectivity anxiety in the fear of having another attack or
of the amygdala with the insula and a reduction agoraphobia, as well as acute paroxysmal fear in
of insular firing, likely mediated by GABA. This the form of panic attacks. Gorman et al. (Gorman,
connectivity and coordination is inhibited in pho- 2000) have proposed a model of diffuse hyperac-
bia patients (Denny et al., 2014). tivity in which both of these symptoms are
In experiential phobia, the model includes accounted for. Brainstem structures such as the
enhanced conditionability and impaired extinc- LC, periaqueductal gray (PAG), and parabrachial
tion (Stein & Matsunaga, 2006), although some nucleus mediate the acute fear response in con-
studies have found no general increase in condi- cert with the hypothalamus, while chronic antici-
tionability in phobia patients compared to con- patory anxiety is mediated via limbic and
trols (Schweckendiek et al., 2011). Extinction in paralimbic structures such as the thalamus,
particular has been studied from a neurochemical amygdala, anterior cingulate cortex (ACC), and
62 L. Havel et al.
insula. The behavioral phenomena of avoidance (Charney et al., 1990). Study findings pertaining
are processed and mediated by cortical areas to serotonin in PD appear to be mixed, but this
such as the PFC with strong ties to the limbic sys- likely reflects the complex nature of anxiety
tem (Sobanski & Wagner, 2017). modulation by serotonin. Early studies of plasma
Reflecting on this neuroanatomical model, the neurotransmitter levels revealed decreased 5-HT
connections to the various neurotransmitter levels (Schneider et al., 1987). In the CNS,
symptoms and their putative roles in PD are clear. 5-HIAA is used as a marker of serotonin turn-
One theory of PD is rooted in hyperactivity of the over. In untreated PD patients, there is evidence
noradrenergic system as it originates in the for increased serotonin turnover, and studies have
LC. Direct stimulation of the LC produces demonstrated that effective treatment leads to
increases in subjective anxiety, somatic symp- decreased CSF 5-HIAA in responding patients
toms, blood pressure, and tachycardia as seen in (Esler et al., 2007). Anti-serotonin and anti-
panic attacks (Heninger & Charney, 1988). receptor antibodies have also been found to be
Furthermore, noradrenergic agonists such as elevated in PD patients (Coplan et al., 1999).
yohimbine have been demonstrated to induce Functionally, 5-HT is known to play a restraint
panic attacks (Charney et al., 1992). The treat- or inhibitory role in the hypothalamus and PAG –
ment of acute panic also relies to some degree on structures that mediate acute fear or panic
a decrease in noradrenergic activity. Reductions (Canteras & Graeff, 2014) – by interacting with
in plasma levels of the norepinephrine metabolite other neurotransmitters such as the endogenous
3-Methoxy-4-hydroxyphenylglycol (MHPG) are opioid system (Graeff, 2017). Furthermore, corti-
seen in parallel with response to treatment with colimbic areas important for anticipatory anxiety
clonidine (Charney et al., 1983). are also sensitive to serotonin transmission via
The LC/NE system is intimately tied to the 5-HT1a and 5-HT2c receptors. Serotonin binding
HPA axis, one of the most important systems for studies have demonstrated abnormal reductions
stress signaling (McCall et al., 2015). Although in 5-HT1a binding in the midbrain and cortex of
many studies have investigated the role of stress patients with PD (Maron et al., 2004a). Studies of
hormones, the results are mixed regarding base- gender differences in PD have shown abnormally
line cortisol, ACTH and CRH, and their response elevated 5-HTT binding in the ACC and midbrain
to induced panic attacks (Bandelow et al., 2017). in males with PD (Cannon et al., 2013).
However, spontaneous panic attacks have consis- Additionally, homozygosity for the short allele at
tently been shown to increase salivary cortisol the serotonin transporter gene may be associated
levels (Bandelow, 2000), and genetic markers of with PD severity (Lonsdorf et al., 2009). Taken
increased HPA activity have been linked to both together, there is evidence of decreased inhibi-
apprehension and post-threat stress responses in tory serotonergic activity in brainstem structures
PD patients (Richter et al., 2012). Atrial natri- important for acute fear and increased activation
uretic peptide (ANP) is a peptide hormone of serotonin systems in corticolimbic areas that
secreted by cardiac tissue that inhibits the release mediate chronic anticipatory anxiety.
of ACTH and cortisol as stimulated by CRH, thus Dopamine (DA) is known to be important
leading to anxiolysis (Ströhle et al., 2001). ANP both in the top-down regulation of the amygdala
is released during both exercise and panic attacks and intrinsic amygdala activity (Grace &
and may play a role in modulating HPA activity, Rosenkranz, 2002). Several studies have studied
likely by decreasing reactivity to calm acute the relationship between DA and PD. Early
panic attacks (Kellner et al., 2001). research demonstrated increased neuroendocrine
Acute fear does not fully encompass PD, how- reactivity to a DA agonist in PD patients com-
ever. Other systems modulate those known to be pared to depressed patients (Pitchot et al., 1992).
hyperactive in panic. One such system is the A small neuroimaging study of females with PD
5-HT system, the importance of which can be found an increased binding potential of the dopa-
inferred from the response to SSRIs seen in PDs mine transporter (DAT) in the striatum in remitted
patients compared to both controls and acutely mechanism for chronic reductions in GABA inhi-
symptomatic patients; likewise, symptom sever- bition could be by stress-induced alterations in
ity was correlated with reduced DAT binding GABA-A receptor modulatory steroid hormones
(Eduard Maron et al., 2010). Most neurobiologi- (Rupprecht, 2003) – including metabolites of sex
cal studies of the dopamine system in PD have steroids such as progesterone which have been
focused on the catechol-O- methyltransferase found to be reduced during panic attacks (Ströhle
(COMT) gene, in particular, the val158met poly- et al., 2003).
morphism, which confers a marked increase in CCK is an important neuropeptide in the fear
the rate of DA breakdown in the CNS. This poly- network (Zwanzger et al., 2012). CCK agonists
morphism has been associated with an increased can reliably produce and induce panic-like
risk for PD (Domschke et al., 2007). Domschke attacks in known PD patients; PD patients appear
et al. (2008) conducted a neuroimaging study to be more sensitive to these agonists (Bradwejn
linking the COMT genotype with functional et al., 1992). Some studies have demonstrated
alterations in PD. Increased amygdala reactivity reduced concentrations of CCK in the CSF of PD
and altered frontal lobe activity were seen in patients compared to healthy controls (Lydiard
response to fearful stimuli in patients carrying at et al., 1992). Genetic studies of the CCK gene,
least one val158met allele. In sum, DA appears to along with CCK receptors and promoters, in PD
reduce acute fear via top-down modulation, patients have demonstrated polymorphisms and
which is reduced or altered in PD patients. mutations associated with the diagnosis (Koefoed
GABA is the most widely distributed inhibi- et al., 2010). Given the lack of treatments target-
tory neurotransmitter in the human brain and is ing the CCK system, this is an area ripe for fur-
particularly important in structures such as the ther clinical investigation.
amygdala that are crucial for fear processing. Finally, one basic molecule in human metabo-
Using magnetic resonance spectroscopy, lism has been extensively studied in PD, carbon
decreased GABA levels have been found in the dioxide (CO2). Panic attacks often include physi-
ACC, PFC (Long et al., 2013), and the occipital cal symptoms suggestive of respiratory dysregu-
cortex (Goddard et al., 2001) in PD. Binding lation. Thus, one theory of PD has been the false
studies have demonstrated decreased GABA suffocation alarm theory (Klein, 1993), which
binding in the insula cortex, which potentially postulates that evolutionarily important “suffoca-
indicates decreased inhibitory tone (Cameron tion alarm” systems are dysregulated or hyperac-
et al., 2007). Hasler and colleagues (2008) found tive, inappropriately cueing the behavioral and
reduced GABA binding potential in the frontal psychological responses to suffocation such as
cortex and increased GABA binding potential in hyperventilation, fight-or-flight, tachycardia, and
the hippocampus and parahippocampal gyrus, others. Panic attacks are reliably induced by
which they suggest is consistent with diminished exposure to increased CO2 concentrations, and
fronto-limbic regulation in PD. Several studies lower relative concentrations are required to
have demonstrated decreased GABA binding in induce attacks for PD patients (Bailey et al.,
the same regions and have indicated a general 2005). In terms of mechanism, many of the previ-
loss of inhibitory GABA tone in these fear cir- ously discussed systems are likely involved in the
cuits (Bremner et al., 2000). Chronic stress – the sensitivity to CO2 seen in PD. Rodent studies
anticipatory anxiety of panic – is known to impair indicate that the amygdala has chemoreceptors
tonic inhibitory GABA circuitry, leading to disin- which detect CO2 concentrations. However, fur-
hibition (Liu et al., 2014) and increased excit- ther human studies found that panic attacks can
atory glutamatergic transmission in the amygdala be induced even in patients with bilateral amyg-
(Masneuf et al., 2014). There is some evidence dala lesions, suggesting an additional, important
that this leads to neuroplasticity changes in the role for brainstem structures (Davis & Whalen,
extended fear network, further contributing to 2001). CO2 may initiate a neurotransmitter cas-
chronic anxiety (Goddard, 2017). One potential cade initiated at the LC; this area has
64 L. Havel et al.
chemoreceptors for CO2 and releases norepi- cyclics such as desipramine) were not (Benkelfat
nephrine to both cardiovascular and emotional et al., 1989). This hypothesis was studied further
control centers, as well as to the HPA axis (Martin using peripheral markers of 5-HT and its metabo-
et al., 2010). This response is further modulated lism. OCD patients with a family history of OCD
by serotonergic systems; studies have demon- had higher baseline 5-HT blood levels than either
strated that 5-HT can inhibit CO2-induced panic OCD patients without a family history or non-
(Schruers et al., 2002), and there is also evidence OCD controls (Hanna et al., 1991). Blood levels
of modulation of the CO2 challenge response by of 5-HT in OCD decreased with medication
serotonin transporter genotype (Schruers et al., treatment (Humble et al., 2001), guiding the
2011). hypothesis of increased serotonin turnover in
OCD. Studies found increased levels of the
marker for serotonin turnover, 5-HIAA, in CSF at
Obsessive-Compulsive Disorder baseline and, similar to 5-HT, a decrease when
treated with clomipramine (Thorén et al., 1980).
Obsessive-compulsive disorder (OCD) is no lon- However, a broader view of the evidence, both
ger formally classified with the anxiety disorders clinical and neurochemical, did not bear out sero-
in the 5th edition of the Diagnostic and Statistical tonergic dysfunction as necessary or sufficient to
Manual (DSM 5) (American Psychiatric explain OCD (Barr et al., 1992). For instance, in
Association, 2013); it has been grouped with one study, the administration of serotonin recep-
other disorders bearing features of compulsive tor agonists (mCPP) and 5-HT precursors (tryp-
behaviors and obsessive cognitive patterns. This tophan) did not produce expected behavioral
change, and the debate surrounding it, reflects the changes or neurochemical responses in either
duality of OCD, both clinically and neurobiolog- controls or OCD patients (Charney et al., 1988).
ically (Hollander et al., 2008; Storch et al., 2008). Indeed, even in positive studies, there are a sub-
On one hand, OCD retains commonality with stantial minority of patients, perhaps up to half,
many anxiety disorders. These similarities that do not respond to serotonin-based treatments
include symptomatology: a high level of baseline (Goodman et al., 1989; Jenike, 2004).
worry and arousal, increased attention to poten- Findings from neuroanatomical research pro-
tially fear-inducing cues in the environment, and tocols have broadened the neurochemical under-
peaks of anxiety and fear when obsessions occur standing of OCD. The current leading model for
or compulsions cannot be performed. They also OCD is rooted in cortico-striatal-thalamo-cortical
include responses to treatment, which in some (CSTC) circuits. This model is supported by find-
ways guided early neurochemical theorizing ings in a myriad of research modalities including
about OCD. However, as reflected by the ulti- lesion reports (Grados, 2003), psycho-
mate removal of OCD from the anxiety disorders immunologic syndromes (Chain et al., 2020),
section in DSM 5, there are many ways in which volumetric analyses (Rotge et al., 2009), func-
OCD is distinct from the other anxiety disorders. tional neuroimaging studies (Brennan & Rauch,
These unique features have driven extensive 2017), and, more recently, outcomes of neuro-
research into the neurobiology of OCD and have modulatory treatments targeting such brain
shed light on the neuroanatomical and neuro- regions (Goodman et al., 2021). These CSTC
chemical underpinnings of the disorder. circuits are driven largely by glutamate, the most
The earliest neurochemical hypothesis of common excitatory neurotransmitter in the adult
OCD focused on serotonin (Stein, 2000). This brain (Saxena & Rauch, 2000). Glutamate is spe-
hypothesis was based on clinicians’ observation cifically implicated in the regulation of motor and
that antidepressants with serotonergic activity cognitive sequences (Karthik et al., 2020).
were effective in OCD (clomipramine, a tertiary Dysfunction in the CSTC circuits is highly sug-
tricyclic antidepressant), while others in the same gestive of a pathogenic role for glutamatergic
class without serotonergic activity (secondary tri- dysregulation in OCD.
Grossly, CSF sampling studies have demon- adjunctive treatments in OCD (Bloch et al., 2006)
strated higher levels of glutamate in the CSF of and provide benefits for related conditions such
OCD patients compared to controls (Chakrabarty as Tourette’s syndrome (Pringsheim et al., 2019).
et al., 2005). However, given the complex nature Furthermore, dopaminergic medications for con-
of glutamatergic signaling, more in-depth inves- ditions such as Parkinson’s disorder and attention-
tigations have attempted to localize this imbal- deficit-
hyperactivity disorder (ADHD) can
ance. These studies, primarily using magnetic unmask repetitive behaviors and cognitions
resonance spectroscopy (MRS), have been less (Borcherding et al., 1990). Medication-naive
conclusive. Early studies of pediatric patients OCD patients show decreased D2 binding poten-
found reduced concentrations of glutamate in the tial in the ventral striatum (Perani et al., 2008).
ACC, which was suggestive of downstream glu- These findings suggest that dopamine hyperac-
tamatergic hyperactivity in the striatum and OCD tivity may be involved in OCD, leading to the
symptomatology (Rosenberg et al., 2004). downregulation of dopamine receptors. However,
Further studies did not replicate these findings theoretically, these observations could also be
regarding the ACC or striatum (Lázaro et al., attributed to low levels of endogenous dopamine.
2012). Our ability to fully characterize the nature Successful deep brain stimulation (DBS) for
of glutamatergic dysfunction in OCD is limited at OCD targeted to the nucleus accumbens (NAc) is
this time, due both to methodological barriers associated with both acute and chronic decreases
(Stanley & Raz, 2018) and confounding factors in binding potential at D2/D3 in the putamen and
such as medication status and comorbidity increased plasma homovanillic acid (HVA), a
(Bédard & Chantal, 2011; Benedetti et al., 2013). metabolite of dopamine. These results suggest
Although local dysregulations in glutamate that effective DBS induces striatal dopamine
transmission that contribute to CSTC dysfunc- release (Figee et al., 2014). Dopamine’s precise
tion have not been demonstrated, the glutamate role in OCD remains unclear, perhaps due to its
hypothesis is further supported by the benefit of complex transmission within striatal structures
certain pharmacotherapies. Interventions that act (Prager & Plotkin, 2019).
to regulate glutamate have shown potential ben- GABA also plays an important role in CSTC
efit in OCD (Pittenger et al., 2011). More recently, circuits, providing top-down inhibition from both
ketamine, an NMDA-R antagonist, has been the prefrontal cortex and striato-thalamic path-
shown to be effective in the acute treatment of ways (Dougherty et al., 2018). MRS studies in
OCD (Rodriguez et al., 2013). Furthermore, OCD have demonstrated decreased GABA in the
SSRI treatment has been found to interact with medial PFC (Simpson et al., 2012) and OFC
the glutamate system. One study found higher (Zhang et al., 2016). GABA levels increased with
levels of total glutamate plus glutamine, choline ketamine infusion and were associated with rapid
(an indicator of neuronal breakdown, perhaps improvement in OCD symptoms (Rodriguez
due to excitotoxicity) in the medial thalamus of et al., 2015). In contrast to other anxiety disor-
OCD patients compared to controls. These levels ders, repeated investigations into the role of the
both declined significantly with effective treat- HPA axis have not demonstrated any consistent
ment with an SSRI (Parmar et al., 2019). This patterns of dysfunction in OCD (Kellner et al.,
interplay is consistent with known actions of 2012). In summary, OCD can be seen as a disor-
serotonin in promoting top-down inhibitory con- der of dopaminergic and glutamatergic dysregu-
trol from the frontal cortex as well as modulation lation in the circuitry that underlies repetitive,
of dopamine and glutamate in the basal ganglia habitual behaviors and the inhibition of those
and thalamus (Dougherty et al., 2018). behaviors. Dopamine and glutamate are likely
The role of dopamine in OCD has also been the primary drivers of hyperactivity in this cir-
investigated. Antipsychotics, including typical cuit, which is modulated by serotonin and, in
antipsychotics with relatively pure and potent D2 turn, GABA.
antagonism, have commonly been used as
66 L. Havel et al.
Conclusion American Psychiatric Association. (2013). Diagnostic

and statistical manual of mental disorders (DSM-5®).
American Psychiatric Publishing.
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Genetics of Childhood
and Adolescent Anxiety 6
and Obsessive-Compulsive
Disorders
Paul D. Arnold, Lilit Antonyan, Francis Routledge,

and Sandra Meier
Anxiety is a part of our lives that allows us to iden- common and associated with significant impacts
tify, prepare, and respond to our environment. on psychosocial functioning and quality of life.
Anxiety can motivate us to deal with challenges In the first section of this chapter, genetic epi-
and provide us with the feelings of worry and demiological approaches including family, high
heightened alertness necessary for survival. risk, and twin studies are briefly reviewed. In this
However, heightened states of anxiety character- section, we also discuss environmental risk fac-
ized by unpleasant feelings of worry and tension tors, which may interact with genetic risk in the
can be maladaptive and result in anxiety disorders. development of anxiety disorders or OCD.
The fifth and most recent edition of the Diagnostics Genetic epidemiological studies have clearly
and Statistical Manual of Mental Disorders (DSM- established the importance of genetic determi-
5) describes anxiety disorders as fear or anxiety nants in anxiety disorders and OCD and provide
responses disproportionate to both the situation an essential backdrop to the second and largest
experienced and the individual’s age, causing sig- section on molecular genetic approaches. In this
nificant impairment or distress (American section, current gene-finding approaches (linkage
Psychiatric Association, 2013). Anxiety is also a and association) are briefly outlined followed by
prominent feature of obsessive-compulsive disor- a comprehensive review of molecular genetic
der (OCD), which according to the DSM-5 is char- findings for anxiety disorders and OCD. The final
acterized by intrusive, recurrent thoughts and section describes novel approaches in psychiatric
repeated, ritualized behaviors (American genetics, including the study of putative endo-
Psychiatric Association, 2013). As noted elsewhere phenotypes, gene-environment interaction, and
in this volume, both anxiety disorders and OCD are genetics of treatment response. The chapter con-
cludes with a brief discussion of anticipated
future trends in the genetics of anxiety and OCD.
P. D. Arnold · L. Antonyan (*) The focus throughout the chapter is on studies
The Mathison Centre for Mental Health Research & of anxiety and OCD in children or adolescents
Education, University of Calgary, Calgary, AB,
Canada
whenever possible. However, relevant adult stud-
e-mail: paul.arnold@ucalgary.ca ies are also summarized from topic areas where
F. Routledge · S. Meier
little is known regarding children, or if the find-
Department of Psychiatry Dalhousie University, ings are clearly of high general relevance to
Halifax, NS, Canada anxiety in all age groups. Given the burgeoning
Department of Psychiatry, Dalhousie University, literature on genetics of anxiety and OCD in
Halifax, NS, Canada recent years, this review is by necessity selective,

https://doi.org/10.1007/978-3-031-14080-8_6
74 P. D. Arnold et al.
highlighting recent and exciting trends in the 2016). Brook and Schmidt (2008) reviewed envi-
literature. ronmental risk factors for developing social anxi-
ety disorder (SAD), a disorder characterized by
persistent fear of social performance and situa-
Evidence from Epidemiological tions. Many environmental risk factors, including
Studies negative pre- and perinatal experiences and gender
roles, were found to contribute to the development
Family Studies Anxiety disorders tend to aggre- of SAD, emphasizing the need for greater consid-
gate in families, suggesting the importance of eration of cultural and societal factors as environ-
genetic risk factors. The risk of developing an mental risk factors. A recent systematic review of
anxiety disorder or OCD in first-degree relatives environmental risk factors for OCD found evi-
of patients with these same conditions is approxi- dence supporting a role for perinatal complica-
mately five times higher than healthy subjects tions, reproductive cycle events, and stressful life
(Hettema et al., 2001; Mataix-Cols et al., 2013; events in conferring risk for OCD (Brander et al.,
Browne et al., 2015). A large population-based, 2016). Another important putative environmental
multi-generational study (over 24,000 probands) risk factor is streptococcal infections, which may
from Scandinavia (Mataix-Cols et al., 2013) found trigger unusually sudden onset of symptoms in a
strong evidence for genetic influences on the lia- subset of childhood onset cases (Swedo et al.,
bility of OCD: the odds ratio (OR) for first-degree 1998). This condition was initially termed Pediatric
relatives was higher than ORs for second- and Autoimmune Neuropsychiatric Disorders
third-degree relatives (ORs 2 and 1.5 for second- Associated with Streptococcal infections
and third-degree relatives, respectively). Although (PANDAS), but more recently was broadened to
OCD has been reported to be significantly more include other infections, and potentially other non-
common in relatives of child compared with adult infectious causes, leading to the designation
onset probands (Nestadt et al., 2000; Pauls et al., Pediatric Acute-onset Neuropsychiatric Syndrome
1995; do Rosario-Campos et al., 2005; Hanna (PANS) (Swedo et al., 2012).
et al., 2005), more recently a large population-
based study (Mataix-Cols et al., 2013) found only
a slightly increased risk in family members of chil- High-Risk Studies A complementary design to
dren with OCD compared with adults, suggesting the family study is a prospective study of “high-
a possible ascertainment bias for earlier studies of risk” individuals, typically the offspring of indi-
children seen in subspecialty clinics. viduals with a disorder. Prospective studies have
indicated that children of anxious parents are at
increased risk of developing anxiety disorders
Environmental Risk Factors Psychological and (Black et al., 2003; Black & Gaffney, 2008;
environmental factors known to influence anxiety Merikangas et al., 2003). In a high-risk study of
symptoms are themselves somewhat heritable children of OCD probands (Black et al., 2003),
(Zavos et al., 2010). Therefore, it is important to 23% of the high-risk offspring met criteria for
consider how the combination of environmental OCD at 2-year follow-up, a proportion signifi-
influences, genetic variation, and the interplay of cantly higher than that for controls. High-risk
these factors drives the development of anxiety offspring were more likely to meet criteria for an
disorders and OCD. Environmental stressors may anxiety disorder generally and scored higher on
increase one’s risk for developing an anxiety dis- dimensional measures of anxiety/depression and
order (Hudson et al., 2019; McLaughin & somatic complaints.
Hatzenbuehler, 2009) or OCD (Brander et al.,
2016). Such environmental factors span social
determinants of health, including low socioeco- Twin Studies In twin studies, monozygotic
nomic status (Beesdo et al., 2009), discrimination, (MZ) and dizygotic (DZ) twin pairs are com-
childhood neglect, and parental conflict (Sederer, pared. MZ twins share 100% of their segregating
6 Genetics of Childhood and Adolescent Anxiety and Obsessive-Compulsive Disorders 75
genes, and DZ twins share 50%. In both cases, model on the genetic level. Studies are consistent
twin pairs are assumed to share the same rearing in that generalized anxiety disorders and panic
environment. Twin studies provide an estimate of disorder (i.e., distress and fear disorders) share a
heritability, a measure of the extent to which genetic basis, whereas at least some subtypes of
genetic factors can explain differences in traits, phobias are influenced by other genetic factors
ranging from characteristics such as eye color (Hettema et al., 2005; Tambs et al., 2009).
and height to psychiatric disorders. Heritability Importantly, the genetic structure of anxiety dis-
estimates range from zero to one, with a herita- orders also changes across development. One
bility closer to zero indicating a trait primarily study supported the distress and fear model in
influenced by environmental factors, while a her- adults, but different structures in younger age
itability estimate closer to one indicates a trait is ranges (Waszczuk et al., 2014).
primarily influenced by genetic factors. Using
heritability estimates derived from twin studies, OCD The best evidence for the heritability of
it is possible to better understand the extent of OCD symptoms comes from large twin studies
variation in anxiety disorders and OCD due to measuring obsessive-compulsive symptoms as
genetics, shared environment, and non-shared quantitative traits distributed continuously
environment. throughout the population, which indicate that
the heritability of obsessive-compulsive symp-
toms is elevated in children (45–74%) compared
Anxiety Disorders Current heritability estimates with adults (27–47%) (van Grootheest et al.,
converge on approximate rates of 35% for gener- 2005; Zai et al., 2019; Burton et al., 2018). A lon-
alized anxiety disorder and approximately 50% gitudinal population-based study on 14,743 twins
for social anxiety disorder, panic disorder, and demonstrated that genetic factors exerted 60–80%
agoraphobia (Meier & Deckert, 2019). The stability over time, with environmental factors
genetic basis overlaps not only within the differ- less consistent over time (Krebs et al., 2015). The
ent anxiety disorders but also with anxiety dimen- same group further found that the correlation
sional traits measured in non-clinical samples, between broader anxiety and OC symptoms is
suggesting at least a partial continuum from nor- r ~ 0.68 and that anxiety sensitivity is a risk fac-
mal to pathological anxiety (Polderman et al., tor for OC traits and vice versa (Krebs et al.,
2015). Importantly, heritability estimates of 2020).
childhood and adult anxiety measures differ
(Polderman et al., 2015). Longitudinal twin stud- In summary, genetic epidemiological
ies suggest that heritability is high in childhood approaches (including family, twin, and high-risk
but decreases over adolescence into adulthood studies) support a substantial genetic contribu-
(Nivard et al., 2015; Waszczuk et al., 2016; tion to anxiety disorders and OCD. A variety of
Hannigan et al., 2017). Genetic effects change environmental risk factors clearly also play a
significantly over the course of child and adoles- substantial role. These studies provide an essen-
cent development (Waszczuk et al., 2016; tial foundation for the molecular genetic studies
Hannigan et al., 2017), but become more stable discussed in the next sections.
over time as individuals reach adulthood
(McGrath et al., 2012).
ene Discovery in Anxiety
G
On the phenotypic level, anxiety disorder sub- Disorders and OCD
types typically fit a two-factor model character-
ized by distress (generalized anxiety disorders Strategies for discovering risk genes have evolved
and MDD) and fear (panic disorder and specific over time, based on available technology and
phobias) (Watson, 2005). Multivariate twin stud- advances in analytic methods. Initially, most
ies have found limited evidence to support this investigators performed linkage studies, genotyp-
ing evenly spaced DNA markers to determine employed to address this issue, for example, test-
chromosomal segments shared by affected indi- ing within families (Ewens & Spielman, 2001).
viduals within families, thereby indicating the Due to the genetic complexity of anxiety disor-
approximate chromosomal location of the sus- ders and other psychiatric disorders, as well as
ceptibility gene(s). Linkage studies, which were the aforementioned methodological issues, can-
very helpful for identifying disorders caused by didate gene studies have had limited success and
single genetic variants of large effect (e.g., low reproducibility (Smoller, 2016; Border et al.,
Huntington’s disease, cystic fibrosis), are known 2019).
to have limited power to detect genetic variants
of small or modest effect (i.e., a relative risk of Anxiety Disorders Studied candidate genes for
less than two) which are more typical of psychi- anxiety disorders are typically found in the
atric disorders and other common complex con- monoaminergic neurotransmitter systems and the
ditions (Risch & Merikangas, 1996). hypothalamic-pituitary-adrenal (HPA) axis.
Genome-wide linkage scans for panic disor- Some of the most commonly studied candidate
der produced mixed findings with the most prom- genes are (1) SLC6A4, particularly the insertion-
ising peaks found within 13q, 14q, 4q, 22q, and deletion polymorphism known as 5HTTLPR
9q (Maron et al., 2010; Smoller, 2008). Genome- (serotonin-transporter-linked promoter region);
wide linkage (GWL) scans of childhood-onset (2) the Val158Met polymorphism (rs4680) of
OCD (Hanna et al., 2002, 2007; Shugart et al., catechol-O-methyltransferase (COMT), a pro-
2006) did not yield significant, replicable find- moter length polymorphism of Monoamine
ings although identification of a linkage peak in Oxidase A (MAOA); and (3) a regulator of G pro-
chromosome 9p24 (Hanna et al., 2002) subse- tein signaling 2 (RGS2) variant (rs4606) (Ask
quently led to multiple findings of associations et al., 2021). Studies examining SLC6A4 (1161
with a biologically plausible candidate gene, the cases vs. 1051 controls) found no consistent
glutamate transporter gene SLC1A1 (as described association with the 5-HTTLPR promoter variant
below). (Meier & Deckert, 2019); however, treatment
prediction based on 5-HTTLPR showed promis-
ing results (Wray et al., 2009).
Candidate Genes
The most well-researched source of genetic vari- OCD Similar to anxiety disorders, the most
ation known to influence the risk of psychiatric studied candidate genetic variant in OCD is
disorders is single nucleotide polymorphisms 5-HTTLPR (Sinopoli et al., 2019; Murphy et al.,
(SNPs). Candidate gene association studies are 2008; Lesch et al., 1996). Meta-analyses of
selected according to limited a priori hypotheses, 5-HTTLPR in OCD have reported either mixed
focusing on the position of the gene under a peak findings (Dickel et al., 2007; Lin, 2007; Taylor,
identified in linkage studies, genomic regions 2013; Walitza et al., 2014) or no association
contributing to anxiety traits in animal models, or between 5-HTTLPR and OCD (Bloch et al.,
the gene’s biological function (Meier & Deckert, 2008; Mak et al., 2015). A possible explanation
2019). The classic design for an association study for the inconclusive findings is the failure of ear-
is based on comparison of allele frequencies in lier studies to consider the rs25531 A/G SNP that
cases and controls. When testing a small number lies within 5-HTTLPR and is known to influence
of genetic variants, a known limitation of the the impact of 5-HTTLPR on expression of the
case-control strategy is the risk of spurious results gene (Hu et al., 2006). Two groups have pub-
in which genetic effects are identified that are lished meta-analyses accounting for the rs25531
unrelated to the disease (population stratifica- variant, and both reported that the LA (high
tion). When candidate gene approaches were the expressing) variant was significantly associated
prevailing paradigm, various approaches were with OCD (Taylor, 2013, 2016; Walitza et al.,
2014). In a meta-analysis, OCD was significantly and glutamatergic genes (e.g., SLC1A1), other
associated with SNPs within another serotoner- genes that have been studied with non-significant
gic gene – serotonin receptor 2A (HTR2A) or mixed findings involve dopamine neurotrans-
(Taylor, 2013, 2016). Like other candidate genes, mission, GABAergic signaling, and brain-derived
findings seem to indicate that HTR2A variants are neurotrophic factor (BDNF) (Zai et al., 2019).
associated with specific OCD subgroups reflect-
ing sex, age of onset, and presence of comorbid-
ity with tic disorders. Genome-Wide Association Studies
The Val158Met polymorphism within COMT This limited success of hypothesis-driven candi-
has been the subject of multiple studies in OCD. date gene studies resulted in the rise of genome-
In a recent meta-analysis of 14 case-control stud- wide association studies (GWAS) that enable the
ies (1435 OCD cases, 2753 healthy controls), this search for risk variants across the genome.
variant was significantly associated with OCD GWAS require many samples to test thousands to
(Kumar & Rai, 2020). Sex-stratified analyses millions of genetic variants. In comparison to
indicated that this association was only found in candidate gene studies, they allow for a more
males (Kumar & Rai, 2020), an observation that detailed search of the genome for genetic
has been made in previous meta-analyses (Taylor, variation.
2013, 2016). GWAS performed in common complex disor-
Glutamate candidate genes have been studied ders have revealed that most common variants
based on evidence from neuroimaging studies have small effect sizes (Sullivan & Geschwind,
and animal models for a role for glutamatergic 2019). According to the common-disease
neurotransmission in pathogenesis of OCD (Wu common-variant hypothesis (Iyengar & Elston,
et al., 2012, Pauls et al., 2014, Rajendram et al., 2007), complex genetic diseases are largely
2017). One of the most reported glutamatergic attributable to common variants of low effect that
genes associated with OCD is SLC1A1 (solute would be amenable to such an approach.
carrier, family 1, member 1) (Arnold et al., 2006; As a result of these small effect sizes, and to
Wu et al., 2012, 2013; Stewart et al., 2013). As overcome the multiple testing burden of examin-
noted above, SLC1A1 is located within the 9p24 ing so many variants, GWAS requires large sam-
region, one of the strongest linkage peaks in ple sizes (thousands of subjects), typically
OCD, and therefore represents an excellent posi- involving multiple collaborative sites.
tional as well as functional candidate for OCD. A
meta-analysis of nine SLC1A1 SNPs in 815 trios, Anxiety Disorders The first GWAS attempt on a
306 cases, and 634 ethnicity- and sex-matched specific anxiety disorder was conducted for
controls (Stewart et al., 2013) yielded largely greater insight into panic disorder. Participants
negative findings with the exception of a single included 200 patients and 200 control subjects
SNP that was modestly associated with OCD from a Japanese population, and several suscepti-
only in males (P = 0.012). The lack of clear asso- bility loci were reported (Otowa et al., 2009).
ciation with common variants could be due to However, a replication study involving more par-
small effect size and phenotypic and/or genetic ticipants failed to replicate the findings from the
heterogeneity. Other glutamate candidate genes previous study (Otowa et al., 2010). A GWAS of
including GRIK2 (Sampaio et al., 2011), GRIN2B 909 patients with panic disorder and 915 controls
(Arnold et al., 2004; Alonso et al., 2012; reported a significant variant in the location of
Kohlrausch et al., 2016), and DLGAP3 (Zuchner transmembrane protein 132D (TMEM132D) on
et al., 2009) have also been studied with mixed 12q24 (Erhardt et al., 2011). Additionally, risk
results. genotypes were associated with higher
In addition to candidate variants within sero- TMEM132D mRNA expression in the postmor-
tonergic genes (e.g., SLC6A4, HTR2A), COMT, tem frontal cortex. Independent SNPs in
TMEM132D were also associated with the sever- sis comprising 192,256 European and 23,074
ity of anxiety symptoms in both patients with African American participants. The study
panic disorder and in patients with depression resulted in six genome-wide loci mapping to the
who were also affected by panic attacks. SATB Homeobox 1 (SATB1), estrogen receptor
1(ESR1), leucine-rich-repeats and IQ motif con-
However, GWAS on specific anxiety disorders taining 3 (LPRIQ3), mitotic arrest deficient 1 like
and anxiety-relevant traits were for a long time 1 (MAD1L1), and transcription elongation factor
severely underpowered and characterized by A2 (TCEA2) genes in the European and the tran-
mostly negative or inconsistent results (Meier & sient receptor potential cation channel subfamily
Deckert, 2019). To overcome sample size limita- V member 6 (TRPV6) gene in the African
tions, researchers started analyzing disorder sub- American subgroup.
types together. By meta-analyzing the results of Leveraging genetic correlations has proved
seven GWAS on five clinically ascertained anxi- successful in increasing the power of GWAS. A
ety disorder subtypes, the ANGST consortium GWAS on latent factors of depressive symptoms
study (Otowa et al., 2016) identified two genome- and anxiety symptoms identified multiple loci
wide significant loci. The first resulted from a (depression: 89 independent variants, 61 genomic
case-control approach (n = 17,310) and mapped loci; anxiety: 102 variants, 73 loci) in the UK
to a non-coding RNA on chromosome 3q12. The Biobank. Of these associated variants, 72% and
second region located in the calmodulin-lysine 78%, respectively, replicated in an independent
N-methyltransferase (CMKMT) gene was associ- cohort of approximately 1.9 million individuals
ated with an anxiety quantitative factor score with self-reported diagnosis of depression and
(n = 18,186). A GWAS making use of the Danish anxiety (Thorp et al., 2021).
national registers (iPSYCH) study including Importantly, GWAS of anxiety phenotypes in
patients with anxiety and related disorders children and adolescents have thus far been
(n = 31,880) identified multiple genome-wide unsuccessful in identifying genome-wide signifi-
significant SNPs mapping to the phosphodiester- cant SNPs (Benke et al., 2014; Jami et al., 2022;
ase 4B (PDE4B) gene (Meier et al., 2019), which Trzaskowski et al., 2013). However, a meta-
has been shown to impact anxiety-like behavior analysis of childhood and adolescent internaliz-
in mice (Zhang et al., 2008). A GWAS on coming symptoms (n = 64,641) by the CAPICE
posite anxiety phenotypes used self-reported consortium identified three significantly associ-
symptoms and diagnoses to create a binary mea- ated genes: WNT family member 3 (WNT3), C-C
sure of lifetime anxiety disorder (n = 83,566) and motif chemokine ligand 26 (CCL26), and centro-
a dimensional measure of current GAD symp- mere protein O (CENPO) (Jami et al., 2022).
toms (n = 77,125) in the UK biobank (Purves OCD: The first GWAS of OCD included 1465
et al., 2020). For lifetime anxiety disorders, five cases and 5557 controls of mixed ages. No
variants reached genome-wide significance with genome-wide significant variants were detected
three implicated in regions coding for the pro- (Stewart et al., 2013). There were also no signifi-
teins neurotrophic receptor tyrosine kinase 2 cant variants identified from the second GWAS
(NTRK2), transmembrane protein 106B based on pediatric onset participants from the
(TMEM106B), and myosin heavy chain 15 OCD Collaborative Genetics Association Study
(MYH15) and two within intergenic regions on (OCGAS) consortium, which included 1065
chromosome 5q15 and 9p23. The largest anxiety families with 1406 affected probands. In this
GWAS to date was performed in 175,163 study, a variant near the gene protein tyrosine
European and 24,448 African US military veter- phosphatase receptor type D (PTPRD) was the
ans from the Million Veteran Program (MVP) strongest finding but did not reach genome-wide
using a 2-item dimensional measure of GAD significance (p = 4.13 × 10−7) (Mattheisen et al.,
(Levey et al., 2020). This GWAS used a binary 2014). Subsequently, a meta-analysis of these
measure of self-reported anxiety disorder diagno- two initial studies, including 2688 cases and
7037 matched healthy controls, did not yield Similar to anxiety disorders, one approach
genome-wide significant loci despite the larger that has been fruitfully applied in OCD genomics
sample size (International Obsessive Compulsive is the analysis of quantitative traits based on self-
Disorder Foundation Genetics Collaborative or parent-report measures of OCD symptoms.
(IOCDF-GC) and OCD Collaborative Genetics The first such study of 6931 samples from the
Association Studies (OCGAS), 2018). The first Netherlands Twin Registry (NTR) tested genetic
sex-stratified OCD GWAS, based on the same associations with scores on the Padua Inventory-
two cohorts, identified two significant associa- Revised and identified a significant association
tions in gene-based analyses that were significant (p = 2.56 × 10−8) with a variant (rs8100480)
only in females, GRID2 (p-value = 2.8 × 10−6) located within MEF2BNB, a gene involved in
and GRP135 (p-value = 8.7 × 10−7) (Khramtsova regulation of expression of muscle specific genes.
et al., 2019). It is important to note that the sam- They also found that a polygenic risk score
ple size of these early studies is much smaller derived from the first GWAS of OCD (Stewart
than the large samples for anxiety disorders noted et al., 2013) predicted OCS in their population-
above and is also much smaller than typical sam- based twin-family sample. SNP-based heritabil-
ple sizes for other psychiatric disorders in which ity was estimated at 14% (Den Braber et al.,
GWAS have identified significant loci (Sullivan 2016). This group later performed a GWAS on
& Geschwind, 2019). Therefore, analyses on the obsession (rumination and impulsions) and
larger samples are needed. Currently, the OCD/ compulsion (checking, washing, and ordering/
Tourette’s Syndrome Working Group of the precision) subscales of the Padua Inventory in the
Psychiatric Genomics Consortium (PGC) is con- NTR (N = 8267). The compulsion subscale
ducting an analysis of a much larger collabora- showed a substantial and significant positive
tive sample. genetic correlation with the OCD case-control
Similar to other psychiatric disorders, GWAS GWAS (rG = 0.61, p = 0.017) performed by the
are revealing extensive shared genetic risk Psychiatric Genomics Consortium (PGC-OCD).
between OCD and other disorders. The shared They did not identify any genome-wide signifi-
genetic etiology between OCD, attention-deficit cant SNPs in their meta-analysis of the PGC and
hyperactivity disorder (ADHD), Tourette syn- NTR data (combined N = 17,992), but aggregate
drome (TS), anxiety disorders, and autism spec- gene-level analyses showed increased enrich-
trum disorders (ASD) has been reported in ment for brain-expressed genes related to psychi-
multiple studies (Davis et al., 2013; Yang et al., atric disorders and increased association with
2021; Yu et al., 2015; Pinto et al., 2016). The gene expression in the amygdala, hippocampus,
cross-disorder group of the PGC performed a and caudate nucleus (brain regions with known
large-scale GWAS with 232,964 cases and roles in emotion, reward processing, memory,
494,162 controls on ADHD, ASD, anorexia ner- and fear) compared to the original PGC-OCD
vosa, bipolar disorder, depression, OCD, TS, and GWAS (Smit et al., 2020).
schizophrenia. They identified 109 risk loci In the “Spit for Science” study, another quan-
shared between at least 2 psychiatric disorders titative trait GWAS was conducted in 5018 unre-
and 23 loci shared between 4 or more disorders lated children and adolescents ascertained in a
(Cross-disorder PGC, 2019). A recent study ana- community setting (at a science museum) and
lyzed cross-disorder genetic associations for TS, assessed using the Toronto Obsessive-Compulsive
ADHD, and ASD (Yang et al., 2021). Using an Scale (TOCS), a novel self- or parent-report
approach guided by genetic correlations, the measure (Park et al., 2016; Lambe et al., 2021).
group identified multiple genetic loci that confer The Rs7856850 SNP in PTPRD was identified as
risks to multiple disorders within this group (a significantly associated (p = 2.48 × 10−8) with
phenomenon known as pleiotropy), including OC symptom severity in the Spit for Science
two pleiotropic regions identified in a meta- sample, and this SNP was also found to be sig-
analysis of OCD and TS. nificantly associated (p-value = 0.0069, same
direction of effect) in a meta-analysis of case- a few CNV and NGS studies have been con-
control datasets (Burton et al., 2021). Polygenic ducted in anxiety disorders and OCD.
risk scores from OC traits were significantly
associated with OCD in case/control datasets and Anxiety Disorders In one recent study, investi-
vice versa (p’s < 0.01). The associated variant gators examined large (>500 kb) CNVs in a
within PTPRD is downstream of the most signifi- cohort from Wales including just over 1000
cant locus in the earlier OCGAS case-control adults with self-reported diagnoses of anxiety or
GWAS described above (Mattheisen et al., 2014). depression and a small comparison group
Taken together, these studies suggest that quanti- (N = 139). They did not find any difference in the
tative symptom data may be useful to find genes rate of large rare CNVs between case and com-
for OCD. As with case-control GWAS, larger parison individuals, enrichment of CNVs previ-
samples are needed to achieve adequate power to ously associated with neurodevelopmental
identify more replicated associations. A group of disorders, or differences based on biological sex
investigators (including two of the authors of this or early reported age of onset (Martin et al.,
chapter, PA and SM) are currently performing a 2021). Using a different approach, another group
GWAS of OC quantitative traits a much larger of investigators found a markedly increase rate of
collaborative dataset. anxiety disorders (47%) and other psychiatric
disorders in adults with CNVs compared with
population rates (Adams et al., 2022).
Studies of Rare Variants
The first whole exome sequencing study of
Many theories have been proposed to explain anxiety disorders was conducted in 54 patients
why variants identified in GWAS are not account- with panic disorder (PD) and 211 control sub-
ing for the heritability observed in twin studies. jects from a Faroe population. The diacylglycerol
Conventionally, GWAS limit analyses to com- kinase eta (DGKH) gene demonstrated the stron-
mon variants (minor allele frequency (MAF) gest association (combined multivariate and col-
≥5%). It is possible that low-frequency lapsing (CMC): p = 1.25 × 10−4) with PD. A
(0.5% ≤ MAF < 5%) and/or rare (MAF <0.5%) smaller whole exome sequencing study on one
variants account for part of the missing heritabil- extended Japanese family, including multiple
ity (Manolio et al., 2009). Data from SNP arrays patients with panic disorders, identified candi-
can also be used to identify rare copy number date genes, of which the phospholipase A2 group
variants (CNVs) and structural rearrangements of IVE (PLA2G4E) gene had the strongest associa-
the genome including deletions, duplications, tion in a follow-up sample of 952 Japanese and
and insertions which are greater than 1 kb in size. 192 German patients and control subjects
Copy number variants have been strongly linked (Morimoto et al., 2018).
to autism spectrum disorder and other neurode-
velopmental disorders (Dinneen et al., 2022). OCD Genome-wide scans have revealed that the
Another type of rare variant, single nucleotide overall burden of rare CNVs does not differ
variants (SNVs) require a different technology between OCD patients and controls. There is
known as next-generation sequencing (NGS), some evidence from these studies for enrichment
which includes targeted sequencing of candidate of genes expressed in brain and genes previously
genes, analysis of all coding variants (whole identified in studies of neurodevelopmental
exome sequencing), or comprehensive analysis disorders (Gazzellone et al., 2016; Grünblatt

of all variants across the genome (whole genome et al., 2017; McGrath et al., 2014). Specific rare
sequencing). Rare CNVs and SNVs can either be CNVs found in OCD patients are in genes or loci
inherited or de novo, which means they are new (including PTPRD, BTBD9, NRXN1, ANKS1B,
mutations that are detected in affected individu- 16p13.11) previously linked to OCD, or com-
als but not in either of their parents. To date, only monly comorbid conditions (Tourette syndrome,
other neurodevelopmental disorders) (Gazzellone family-based and case-control samples). In case-

et al., 2016; Grünblatt et al., 2017; McGrath control comparison cases (n = 1263 cases and
et al., 2014). 11,580 controls), the most significant single-gene
result was for SLITRK5 (OR = 8.8, p = 2.3 × 10−6),
The gene SLITRK1 was originally studied as a interesting given the findings for another func-
candidate gene for Tourette Syndrome (TS) based tionally related gene (SLITRK1) noted above.
on its proximity to a chromosomal inversion in a Analysis of trios identified an increase rate of de
child with TS, the subsequent discovery of other novo variants predicted to be damaging
rare variants in individuals with TS, and the (Halvorsen et al., 2021).
absence of such variants when screening control In summary, next-generation sequencing stud-
chromosomes (Abelson et al., 2005). Given the ies of anxiety disorders are too small to draw con-
phenotypic overlap between TS, OCD, and clusions regarding the role of rare variants in
related disorders (e.g., trichotillomania), investi- these conditions. In contrast, recent advances in
gators subsequently sequenced the complete cod- OCD from larger samples indicate the potential
ing region of genes in adults with OC spectrum involvement of rare variants in the pathogenesis
disorders (381 cases) and 356 controls, which of this disorder. Future sequencing studies of
suggested the possible involvement of novel rare larger samples sizes, potentially including newer
SLITRK1 variants in OC spectrum disorders technologies such as whole genome sequencing,
(Ozomaro et al., 2013). will shed more light on the contribution of rare
Another group applied a novel, cross-species variants to anxiety disorders and OCD.
approach and selected 608 candidate genes based
on three sources of information: (1) a previous
GWAS of a canine model of OCD (Tang et al., Gene by Environment Interplay
2014), (2) genes previously associated with
autism spectrum disorders, and (3) hypothesis- The involvement of gene-environment interac-
driven candidate genes for OCD (including many tions (G × E) in driving the genetic risk for and
of the genes described above). They then per- pathogenesis of anxiety disorders has been
formed targeted sequencing on 592 OCD patients explored in a considerable body of literature.
and 560 controls. Four genes (NRXN1, HTR2A, Recently, large gene-environment-wide interac-
CTTNBP2, REEP3) were identified as having an tion studies (GEWIS) were performed using the
increased burden of functionally significant vari- UK Biobank cohort (n = 371,903–432,881). A
ants in OCD cases compared with controls. All GEWIS examining the risk of maternal smoking
four genes are involved in neurotransmission and during pregnancy (MSDP) and offspring’s anxi-
synaptic connectivity within cortico-striatal- ety and depression (Chu et al., 2021) revealed a
thalamo-cortical (CSTC) circuits implicated in significant finding for the Unc-80 Homolog
OCD. When comparing with sequencing data (UNC80) gene and anxiety. A GEWIS on socio-
from 33,379 population-based controls, NRXN1 economic factors based on Townsend deprivation
was highly significantly associated with OCD: index data identified several candidate genes as
p = 6.37 × 10−11 (Noh et al., 2017). interacting with socioeconomic factors (Ye et al.,
Recently, two whole exome sequencing stud- 2021). Lastly, a GEWIS identified multiple genes
ies have been performed in OCD. The first study that interacted with long-term antibiotic use in
involved family-based exome sequencing of 222 early life in their association with adult mental
OCD parent-child trios and 777 previously health traits, including ANK3 for anxiety (Liang
sequenced unaffected trios. Damaging de novo et al., 2021).
variants were identified in the genes CHD8 and For OCD, a candidate gene-by-environment
SCUBE1 (FDR q-value <0.1) (Cappi et al., 2020). study focused on the interaction between early
In a larger study, whole exome sequencing was adversity as measured using the Childhood
performed on 1313 total cases (including both Trauma Questionnaire (CTQ) and variants within
COMT, monoamine oxidase A (MAOA), and Anxiety Disorders Previous studies on methyla-
monoamine oxidase B (MAOB). This study tion alterations in anxiety disorders have mostly
revealed that childhood trauma interacted with focused on candidate genes putatively involved
haplotypes in all three genes, increasing risk of in stress response, neurotransmission, and neuro-
OCD (McGregor et al., 2016). plasticity (Schiele & Domschke, 2018).
These environmentally contingent genetic Unfortunately, most of these studies were under-
effects point to a promising future for GxE powered to detect a signal that survives multiple-
studies. However, it is essential to consider the testing correction (Schiele & Domschke, 2018).
reliability of G × E findings due to their limited
scope. Limitations in both sample size and con- Recent advancements in technology now
ceptualization of environmental risk assess- enable the examination of DNA methylation pat-
ment pose challenges in conducting G × E terns on a genome-wide level. Global DNA
studies. An estimated sample size of 10,000 methylation alterations have been reported in
participants is minimally necessary to detect individuals with anxiety symptoms at a subclini-
moderate G × E significance (Uher, 2014), and cal level (Murphy et al., 2015). In a large cohort
G × E studies have focused on functional candi- (N = 1522), significantly increased DNA meth-
date markers within a limited number of genes. ylation at a single CpG site in the promoter of the
Additionally, defining environmental exposure ASB1 gene correlated with high levels of general-
and timing of exposure is challenging (Klauke ized anxiety symptoms (Emeny et al., 2018). An
et al., 2010). epigenome-wide association study (EWAS)
assessing more than 480,000 cytosine residues
found panic disorder to be associated with sig-
Epigenetics nificant differential DNA methylation (hypo-
methylation in most instances) at 40 CpG sites, in
Epigenetics is involved in various biological phe- patients compared with controls (Shimada-
nomena, including gene expression and cell dif- Sugimoto et al., 2017). In another EWAS includ-
ferentiation (Portela & Esteller, 2010). Epigenetic ing 89 medication-free patients with panic
modifications can be long-lasting, but also tem- disorder and 76 healthy controls stratified by gen-
porally highly dynamic and responsive to envi- der, one locus with genome-wide association was
ronmental factors, and can alter gene regulation detected in an enhancer region of the HECA
and expression. Such modifications include DNA gene, specific to female patients. The same locus
methylation (mDNA) at cytosine (CpG) sites, was found to be hypermethylated in a female rep-
which can alter DNA binding to regulatory pro- lication sample. In addition, methylation at this
teins, and histone acetylation and methylation at CpG site was associated with HECA mRNA
specific amino acids that alter chromatin avail- expression in another independent female sample
ability for transcriptional activity (Huang et al., (n = 71), both at baseline and after induction by
2014). Unlike genomic DNA, epigenetic changes dexamethasone (Iurato et al., 2017). In an EWAS
can be tissue-specific, an important consideration of 66 patients with social anxiety disorder and 77
when comparing results from studies that are healthy controls, genome-wide associations were
based on different sample types (e.g., saliva vs. observed in exon 4 of the Tenascin XB (TNXB)
blood). Epigenetics has been suggested to play a gene and the intron of the solute carrier family 43
key role in the pathogenesis of anxiety disorders member 2 (SLC43A2) gene. Strikingly, hypo-
and OCD at the intersection of genetic and envi- methylation of TNXB was consistent with results
ronmental factors (Klengel & Binder, 2015) and from the EWAS of panic disorder (Shimada-
may be a possible explanation for the observed Sugimoto et al., 2017) described above. Similarly,
missing heritability (Trerotola et al., 2015; changes in the differential DNA methylation of
Bourrat et al., 2017) in genetic studies of these SLC43A2 have been described in response to
disorders. cognitive-behavioral therapy in patients with
panic disorder (Ziegler et al., 2019). Accordingly, hypomethylated compared with controls, but the
these shared associations point towards more differences were small compared with the other
general epigenetic effects in the pathogenesis of disorder groups (Siu et al., 2021). Overall, there
anxiety disorders. has been some inconsistency with findings on
OXTR methylation levels in OCD, which can be
OCD To date, there are a limited number of epi- at least partially explained by low sample power
genetics studies for OCD pediatric samples. The as well as varying tissue types (e.g., blood vs.
first study on DNA methylation profiles in OCD, saliva).
focusing on 14 candidate genes previously asso- In an EWAS of 65 OCD affected and 96 unaf-
ciated with the disorder, was conducted on neo- fected individuals, 2190 unique differentially
natal blood spot samples from 33 female children/ methylated genes were identified. Among these
adolescent subjects (21 cases, 12 controls). There differentially methylated genes, a number had
were no statistically significant results reported; been identified in previous genetic or epigenetic
however, preliminary results provide evidence studies of OCD including BCYRN1, BCOR,
for differential methylation profiles of the GABA FGF12, HLA-DRB1, and ARX (Yue et al., 2016).
B receptor 1 (GABBR1) and myelin oligodendro- In another EWAS of saliva DNA, 59 children
cyte glycoprotein (MOG) genes (Nissen et al., affected with OCD were compared with 22 chil-
2016). dren with ADHD and 54 controls. In this study,
DNA methylation differences from controls were
Other candidate methylation studies have more readily identified in patients with higher
focused on single genes. As with candidate stud- symptom severity (in both the OCD and ADHD
ies of genetic variants, SLC6A4 has been a focus groups) (Goodman et al., 2020).
for methylation studies (Schiele et al., 2021a, b;
Grünblatt et al., 2018). One study found that
DNA methylation levels of SLC6A4 in an ampli- Endophenotypes
con located at the beginning of the first intron
were significantly higher in the saliva of pediatric One alternative approach to studying genetics of
OCD patients compared to controls and adult anxiety disorders and OCD is the study of endo-
patients with OCD (Grunblatt et al., 2018). A phenotypes. A strict definition of endophenotype
more recent study reported that hypermethylation requires certain criteria be met, including herita-
of the SLC6A4 promoter may be a good indicator bility, state-independence, co-segregation within
of impaired treatment response (Schiele et al., families, and greater frequency in unaffected
2021b). family members compared with the general pop-
Oxytocin, a hormone linked to emotional regulation (Gottesman & Gould, 2003).
ulation and attachment, has been the subject of a Endophenotypes have been suggested from mul-
few candidate gene methylation studies in small tiple sources including cognitive tasks, physio-
samples of individuals with OCD (Cappi et al., logical measures, and neuroimaging (Domschke
2016; Schiele et al., 2021a; Park et al., 2020; Siu & Dannlowski, 2009).
et al., 2021). Hypermethylation of the oxytocin One particularly promising endophenotype is
receptor gene (OXTR) was observed in two stud- error-related negativity (ERN), an electrophysio-
ies (Cappi et al., 2016; Schiele et al., 2021a), logical marker measured using electroencepha-
whereas hypomethylation was observed in lography (EEG). The ERN, a negative deflection
another study comparing OCD cases with healthy in the event-related potential following an
controls (Park et al., 2020). Another study by Siu incorrect response during a performance of a task,
et al. observed altered methylation levels of is a putative mechanistic biomarker of anxiety
OXTR in pediatric subjects with primary diagno- across the lifespan. The ERN has been associated
ses of ASD, ADHD, and OCD. In this study, chil- with OCD and OC traits in adults and children
dren with OCD had some CpG sites that were (Carrasco et al., 2013b; Gehring et al., 2000;
Bernstein et al., 1995; Mathews et al., 2012; 2022). Endophenotype studies, in which unaf-
Hanna et al., 2018) and with pediatric generalized fected relatives are studied to identify potential
anxiety disorder (Hanna et al., 2020). It is likely heritable structural or functional brain altera-
that ERN is transdiagnostic, and not specific to tions, have involved smaller samples and have
either OCD or anxiety disorders, as evidenced, for not resulted in consistently replicated findings.
example, by its association with withdrawn/ Future studies, such as a new global study includ-
depressed behaviors in children with OCD (Hanna ing 100 unaffected adult siblings of individuals
et al., 2016). ERN is elevated in the first-degree with OCD (as well as 250 medication-free adults
relatives of individuals with both OCD and GAD and 250 healthy controls), should help address
(Carrasco et al., 2013a; Riesel, 2019) and, there- this gap in our knowledge (Simpson et al., 2020).
fore, meets the requirement that endophenotypes However, this study does not include children
be heritable. The ERN has been described as an and adolescents, which is true of most neuroim-
excellent example of the Research Domain aging endophenotype studies to date. A notable
Criteria (RDOC) of NIMH (Hanna & Gehring, exception is a mixed adult and adolescent study
2016). Furthermore, an imaging study provided that identified structural changes within
preliminary evidence that structural brain altera- orbitofronto-striatal and posterior brain circuitry
tions in an extended network for error processing in patients with OCD, which were shared with
are linked to the ERN (Liu et al., 2014). unaffected relatives, compared with controls
There are a number of neurocognitive corre- (Shaw et al., 2015).
lates of pediatric OCD, representing candidate Even without established heritability, imaging
endophenotypes such as decision-making (Ozcan phenotypes have been studied for their associa-
et al., 2016), planning (Bey et al., 2018), response tion with candidate genetic variants in children
inhibition (Mar et al., 2022), memory (Zhang with OCD. Preliminary associations have been
et al., 2015a), reversal learning (Tezcan et al., reported with various glutamate and serotonin
2017), and cognitive flexibility (Ozcan et al., system genes and structural and functional altera-
2016) (reviewed in Marzuki et al., 2020). Two tions within corticostriatal circuits based on a
recent, methodologically rigorous studies tested range of neuroimaging modalities (Arnold et al.,
neurocognitive endophenotypes in OCD pro- 2009a, b; Gassó et al., 2015; Ortiz et al., 2016;
bands, together with unaffected siblings and/or Sinopoli et al., 2020); however, such findings
parents. The results differed, with one study iden- have not replicated across studies. Future studies
tifying deficits shared by OCD proband and unaf- should be conducted using genome-wide
fected relatives in cognitive flexibility and approaches, in sufficiently large samples. Another
response inhibition (Abramovitch et al., 2021), promising approach is testing whether polygenic
and the other in planning (Negreiros et al., 2020). risk scores (PRS) for OCD or other disorders pre-
Another small study focused on “high-risk” (HR) dict imaging endophenotypes. One example of
children who were siblings or children of indi- this approach can be found in a recent study, in
viduals with OCD and who exhibited subclinical which investigators reported that PRS for OCD
obsessive-compulsive symptoms but not did not predicted brain response during working memory
meet diagnostic criteria for OCD. They identified in individuals with OCD and unaffected relatives,
statistically significant performance deficits in but not in controls (Heinzel et al., 2021).
spatial working memory in HR children com-
pared with controls (Bernardes et al., 2020).
Great advances have been made in recent Genetics of Treatment Response
years in defining neuroimaging correlates of anx-
iety and OCD, and as with other psychiatric dis- Pharmacogenetics studies have been conducted
orders, analyses of large neuroimaging cohorts in OCD, mostly focused on genes in the cyto-
have been accelerated through the ENIGMA con- chrome P450 system, involved in liver metabo-
sortium (Harrewijn et al., 2021; Heuvel et al., lism of SSRIs (Zai et al., 2014; Elliot et al., 2017;
Müller et al., 2012; Brandl et al., 2014). CYP2D6 otype on categorical or dimensional anxiety out-
and CYP2C19 genes have been studied in multi- comes (Schiele et al., 2021c). Future studies
ple adult OCD studies (Müller et al., 2012; should examine whether other genetic variants,
Brandl et al., 2014). In particular, a study involv- polygenic risk scores, or epigenetic factors mod-
ing 184 OCD adult cases showed that genetic erate therapy outcome in anxiety disorders or
variants associated with poor CYP2D6 metabo- OCD.
lism are highly correlated with antidepressant Although little is known to date about the
side effects, specifically with side effects from genetics of treatment response in anxiety disor-
venlafaxine (Brandl et al., 2014). ders and OCD, more findings are likely to accu-
Serotonergic and glutamatergic genes have mulate in the coming years, holding out the
also been the subject of antidepressant treatment prospect of identifying genetic predictors that
response studies (Zai et al., 2014, 2019). A study will enable better tailoring of treatment to indi-
of treatment response in adults with OCD found vidual patients.
a significant association between the rs6305 vari-
ant in HTR2A and non-response (Corregiari et al.,
2012). SLC1A1 has also been investigated in Conclusions and Future Directions
pharmacogenomic studies (Bandelow et al.,
2016; Zhang et al., 2015b; Real et al., 2010). The The rapid pace of technological advance and
rs301434 variant of SLC1A1 was significantly more advanced analytic methods are expected to
associated in one study with both SSRI nonre- revolutionize molecular genetic studies over the
sponse and fluoxetine response (Zhang et al., next decade. Currently, the emphasis is on
2015b). Furthermore, another two variants genome-wide association studies using ever
(rs2228622 and rs3780413) of SLC1A1 were larger samples. More publications based on
associated with fluoxetine response in another whole exome and whole genome sequencing
study (Abdolhosseinzadeh et al., 2019). approaches are also expected in the coming years.
Leveraging data from one of the GWAS Findings based on GWAS and next-generation
described above, investigators tested association sequencing should lead both to identification of
with medication response in 804 mixed adult and biological pathways underlying OCD and
pediatric patients diagnosed with OCD. The most improvement in risk prediction models using
significant variant in this analysis was rs17162912 polygenic risk scores combined with non-genetic
(P-value = 1.76× 10−8) which is near DISP1. predictors. However, currently PRS approaches
Further enrichment analysis showed a suggestive are significantly limited by the fact that the sam-
association between OCD treatment response ples from which they are derived consist almost
and genes involved in glutamatergic and seroto- entirely of individuals of European ancestry.
nergic neurotransmission (Qin et al., 2016). A Therefore, increasing diversity of participants is
subsequent study which sought to replicate the becoming a major emphasis in psychiatric genet-
association of DISP1 with OCD treatment ics, and it is hoped that more ethnically diverse
response in an independent sample was negative samples will in turn lead to increased clinical
(Lisoway et al., 2018). utility of PRS approaches in people from all
A number of studies have also examined ancestral backgrounds (Peterson et al., 2019).
whether the 5-HTTLPR variant moderates SNP-based strategies will be complemented by
response to cognitive-behavioral therapy in indi- study of copy number variation and epigenetic
viduals with anxiety disorders. Findings have approaches which will reveal different biological
been mixed, and a recent meta-analysis of 2195 mechanisms underlying anxiety disorders and
individuals with anxiety disorders attempted to OCD.
determine whether there was any consistency Endophenotypes, such as neurocognitive tasks
across studies. The results of this meta-analysis and brain imaging abnormalities, also represent
revealed no significant effects of 5-HTTLPR gen- promising phenotypes for genetic studies, as do
quantitative symptom measures. Future studies & neuroscience: JPN, 37(4), 273–281. https://doi.
org/10.1503/jpn.110109
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Arnold, P. D., Rosenberg, D. R., Mundo, E.,
it may take many years to fully elucidate how Tharmalingam, S., Kennedy, J. L., & Richter, M. A.
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genetics of drug response is likely to result in receptor gene (GRIN2B) with obsessive-compulsive
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Taxometric Methods in Child
Christian A. Hall and Joshua J. Broman-Fulks
Approximately one-third of US adolescents have One issue that permeates the anxiety literature
experienced symptoms of an anxiety disorder at and informs everything from the theoretical con-
some point in their lives (Kessler et al., 2012) and ceptualization of anxiety disorders to appropriate
an estimated 7.1% of US youth aged 3–17 cur- assessment approaches and treatment targets
rently meet diagnostic criteria for an anxiety dis- regards the latent structure of anxiety and anxiety-
order (Ghandour et al., 2019). The worldwide related concerns. Latent structure refers to
prevalence of anxiety disorders in child and ado- whether anxiety disorders represent naturally
lescent populations is similarly high (i.e., 6.5%; occurring taxa (i.e., categories) that are distinct
Polanczyk et al., 2015) and appears to be increas- from one another, other psychological disorders,
ing over time, especially among adolescent and normality, as is implied by the categorical
females (Bor et al., 2014). This is a worrisome approach represented in the DSM-5 diagnostic
trend, as an anxiety disorder diagnosis during system, or whether these disorders represent con-
adolescence is a predictor of future suicidal ide- tinuous variations along one or more relevant
ation, chronic stress, substance use, and low dimensions. Fortunately, there is an empirical
well-being, among other forms of psychological approach that can inform discussions of latent
suffering (Essau et al., 2014). Despite the exis- structure known as taxometrics. In this chapter,
tence of efficacious interventions targeting child we will present a comprehensive review of the
and adolescent anxiety disorders (see Higa- taxometric literature as it pertains to anxiety and
McMillan et al., 2015), anxiety-related suffering anxiety-related concerns. We will begin by dis-
in youth remains a public health issue of signifi- cussing some issues with the classification of
cant cost and burden at the individual and societal anxiety disorders under current diagnostic sys-
levels (Olfson et al., 2012; Wittchen, 2002). To tems and outline the history, practice, and appli-
address this issue, it is imperative that researchers cation of taxometric methods as they pertain to
and clinicians work collectively to develop evi- these issues. Then, we will review the literature
dence-based theoretical models and efficacious of taxometric research on child and adolescent
strategies for the assessment, diagnosis, and anxiety disorders and related constructs, includ-
treatment of anxiety disorders. ing several relevant transdiagnostic features and
risk factors, and we will discuss what can be
C. A. Hall · J. J. Broman-Fulks (*) inferred from taxometric studies of anxiety-
Department of Psychology, Appalachian State related constructs in adults. The chapter will con-
University, Boone, NC, USA clude with a summary, recommendations for
e-mail: bromanfulksj@appstate.edu

https://doi.org/10.1007/978-3-031-14080-8_7
98 C. A. Hall and J. J. Broman-Fulks
researchers and clinicians, and a reflection on the comorbidity across a spectrum of mental health
state of the field of taxometrics as it concerns the disorders raises concerns about the validity and
study of child and adolescent anxiety disorders. utility (Ghaemi, 2016) of diagnostic boundaries
between mental disorders (Allsopp et al., 2019;
Jablensky, 2016; Rutter & Pickles, 2015).
Classification Assuming for the moment that child and ado-
lescent anxiety disorders are categorically struc-
Anxiety disorders, characterized by the experi- tured diagnostic entities, one must ask from
ence of excessive and impairing fear and worry, which causal mechanisms (e.g., dichotomous
can be examined at multiple levels of analysis. genetic factor, threshold-dependent effect, or
The Diagnostic and Statistical Manual (DSM-5; interaction effect) these disorders emerge (Ruscio
American Psychiatric Association, 2013) et al., 2011). In many cases, etiological knowl-
describes anxiety disorders as collections of edge is necessary for the differential diagnosis of
symptoms that include markers of sympathetic symptoms common to multiple disorders. For
arousal (i.e., increased heart rate, sweating, ten- example, the presence of an underlying medical
sion), anxious cognitions (i.e., nervousness, condition, such as arrhythmia, asthma, irritable
worry, fear), and behavioral responses that func- bowel syndrome, or hyperthyroidism, may dis-
tion to reduce or eliminate these unwanted expe- tinguish justified reactions to associated physical
riences. Whether these “symptoms” are sensations from the often-unfounded sensitivities
attributable to discrete patterns of genetic expres- of GAD or panic disorder (Jordan & Okifuji,
sion, specific events in childhood, learned behav- 2011; Meuret et al., 2017). Likewise, anxiety and
iors, or interactions between such variables externalizing disorders can be differentiated
remains an etiological concern unaddressed by when symptoms common to both diagnoses (i.e.,
the diagnostic system. Though some risk factors inattention, restlessness, etc.) are understood in
for child and adolescent anxiety disorders have the context of the processes specific to either dis-
been identified, such as parenting style (e.g., order from which they emerge. For example,
Möller et al., 2016) and temperament (e.g., avoidance due to excessive worry may be an indi-
Degnan et al., 2010), individual differences in cator for anxiety, while avoidance in opposition
development and a multitude of other biological to requested involvement in a family activity may
and environmental factors complicate causal be an indicator for an oppositional defiant disor-
explanations for the development of anxiety dis- der (Freidl et al., 2017). When unavailable to cli-
orders (Creswell et al., 2014; Mian et al., 2011). nicians, the history and timing of symptom
For clinicians working with youth, the differ- development may pose additional challenges in
ential diagnosis of anxiety disorders poses addi- diagnosis. For example, the presence of social
tional challenges (Freidl et al., 2017). Child and fear can be used to differentiate SAD from an
adolescent anxiety disorders share many sympto- autism spectrum disorder when common symp-
mological features with other diagnoses, such as toms like social impairment and avoidance com-
mood, somatoform, and substance use disorders, plicate diagnosis. A child with autism may learn
making it difficult to distinguish between discrete to develop social fears not initially present after
classes of disorder (Jarrett et al., 2012; Kendall experiencing the negative consequences of social
et al., 2010). In addition, anxiety disorders in impairment. Consequently, the presence of social
youth are also frequently comorbid with mood fear may only be useful as a diagnostic tool when
disorders, medical conditions, autism spectrum clinicians can chart its course through develop-
disorders, externalizing disorders, and one ment (Tyson & Cruess, 2011).
another, further complicating diagnosis (Beesdo In final consideration to the question of why
et al., 2009; Cummings et al., 2014; Kerns et al., one should care about the latent structure of child
2016; Reale et al., 2017; Verduin & Kendall, anxiety disorders, Beauchaine (2003) outlines
2003). These patterns of symptom overlap, and five major points that are only briefly summa-
7 Taxometric Methods in Child and Adolescent Anxiety Disorders 99
rized here. First, understanding the structure of ics, that can be applied to proposed indicators
anxiety disorders that emerge early in develop- (e.g., symptoms) of a construct.
ment can inform risks for the development and Although a detailed explanation of taxometric
maintenance of other disorders into adulthood. methodology is well beyond the scope of this
Second, diagnostic systems still in use today chapter, a general understanding of how taxomet-
(e.g., the DSM-5 and ICD-10) are plagued by ric procedures function and how their results are
assumptions and distinctions that lack empirical interpreted may aid the reader. In short, the pro-
support and hold significant implications for cedures Meehl developed represent different
treatment. Third, taxometric research has the ways of evaluating the statistical relationships
potential to reveal periods in development during among two or more prospective indicators of a
which pathological traits and other risk factors construct along moving cuts (e.g., scores) of
are likely to emerge. Fourth, categorical differ- another indicator. The resulting relationships can
ences may exist between groups that determine be plotted and the shape and consistency of the
or influence response to treatment. Taxometric plots examined. In general, plots of the relation-
analyses would enable clinicians to identify these ships between indicators of a categorical con-
groups and plan treatments accordingly. This struct will exhibit a characteristic shape (e.g., a
would be especially helpful in cases where cer- bimodal distribution, convex upward) that is dis-
tain treatments may be contraindicated by mem- tinct from plots produced by dimensional vari-
bership to a latent group within the population of ables (e.g., a unimodal distribution, concave
treatment seekers. Finally, distinguishing downward). Rather than rely upon null hypothe-
between dimensional and taxonic constructs can sis testing, the taxometric method employs mul-
enable researchers and clinicians to chart the tiple consistency tests, and the fit of the plots
developmental pathways of anxiety disorders. generated by the data of interest is compared to
Whether a disorder emerges at the end of a multi- Monte Carlo simulations of categorical and
faceted causal pathway (equifinality) or marks dimensional plots. While early taxometric proce-
the emergence of a variety of pathways that may dures relied heavily on the subjective visual inter-
or may not result in the disorder (multifinality), pretation of plots, most modern taxometric
knowledge of its structure is essential in under- analyses employ an objective fit index (i.e., the
standing its development across time. Comparison Curve Fit Index, or CCFI; Ruscio,
2007) when interpreting whether the resulting
data plots are more consistent with a categorical
Taxometrics or dimensional model. CCFI scores range from 0
to 1, with lower CCFI values (<0.45) imparting
The detection of latent clinical classes (i.e., taxa) greater confidence that the construct of interest
through empirical means was pioneered by Paul has a dimensional latent structure and higher
Meehl, a clinical psychologist and philosopher of CCFI values (>0.55) suggesting a categorical
science who assembled a comprehensive method latent structure. CCFI values ranging from
for taxometric analysis (Meehl & Golden, 1982). approximately 0.45–0.55 are considered too
At the time, it was widely assumed and codified ambiguous to support either claim, though this
into diagnostic manuals that mental illness was to range can vary in stringency (Ruscio et al., 2010).
be diagnosed as a distinct state of impairment – An understanding of CCIF score interpretation
you either “have it or you don’t” – contrary to will be useful throughout this chapter as a means
healthy or otherwise normal states of being to interpret the results of taxometric studies. For
(Mayes & Horwitz, 2005). Observing the absence additional information, Beauchaine (2007) and
of empirical support for such assumptions, Meehl Ruscio et al. (2011) provide excellent primers for
developed a set of nonredundant statistical proce- taxometric analysis that further detail its theory
dures, collectively known as coherent cut kinet- and application.
axometric Findings for Children

T 5–16 (Liu, 2016; Slade & Andrews, 2005). In
and Adolescents light of these studies, MAD may have exhibited a
taxonic structure in the data collected by Schmidt
To date, only two studies have directly examined et al. due to features specific to the anxiety con-
the latent structure of anxiety-related constructs struct, or to an interaction between anxiety and
among child and adolescent samples using taxo- depression. It is also plausible that the indicators
metric methodology. The first, conducted by used in their analyses were more indicative of an
Schmidt et al. (2007), applied taxometric proce- unidentified construct underlying both anxiety
dures to discern the structure of mixed anxiety and depression. Overlapping symptomatology
depression (MAD) for its consideration as a diag- and shared biological mechanisms provide theo-
nostic category. In this study, three large cohorts retical justification that a common feature of both
of adolescent participants were randomly selected anxiety and depression might categorically dis-
from high schools in Oregon to complete mea- tinguish the combination of these disorders from
sures of self-report, parent-report, and clinician- normal functioning (Galyamina et al., 2017).
rated symptoms of anxiety and depression at two The only other study to date applying taxo-
time points, separated by a little over a year. metric methods to child and adolescent anxiety
Indicators from these measures were subjected to disorders was conducted over a decade ago.
two taxometric procedures, the results of which While investigating the structure of posttraumatic
were both interpreted as supporting the existence stress disorder (PTSD) in a national sample of
of a MAD taxon representing approximately over 2800 adolescents, Broman-Fulks et al.
13% of the adolescent population. Additional (2009) subjected indicators representing three
non-taxometric modeling procedures also sup- PTSD symptom clusters (re-experiencing, avoid-
ported a categorical model of MAD with an esti- ance/numbing, and hypervigilance) to taxometric
mated taxon base rate of approximately 12%. analysis. The results, which included CCFI
One-third of students predicted to belong to the scores of 0.20 and 0.23 across two non-redundant
taxon class met criteria for a diagnosis of an anxi- procedures, provided strong support for a dimen-
ety or mood disorder at the first time point, and sional model of PTSD symptomatology within
by the second time point, those students who the youth sample. This dimensional conceptual-
were thought to belong to the MAD taxon ization of PTSD was also supported through tax-
reported increased scores on measures of depres- ometric investigations in adult samples (Ruscio
sion, anxiety, and worry. et al., 2002; Forbes et al., 2005; Broman-Fulks
All in all, Schmidt and colleagues initiated the et al., 2006). Though commonly associated with
search for the structure of anxiety disorders in a specific traumatic event, taxometric evidence
adolescents with strong support for the categoric- suggests that PTSD symptomatology is not cate-
ity of mixed anxiety depression. However, it is gorically different from “normal” responses to
unclear to what extent these findings more extreme stressors.
broadly represent anxiety disorders in the absence Similar findings have emerged from taxomet-
of comorbid depression. Two years prior, Hankin ric studies of constructs implicated in the etiol-
et al. (2005) used indicators from both youth and ogy and symptomology of anxiety-related
parent reports of depression symptoms in a large concerns among children and adolescents. For
sample of children and adolescents to identify the example, anxiety sensitivity (AS), or the fear of
latent structure of depression. Consistent across anxiety-related sensations, is a known vulnerabil-
report-type, construct domain, and demographic ity factor for the development and maintenance
variables, their analyses aligned to suggest that of anxiety disorders. Bernstein et al. (2005,
depression was best represented as a dimensional 2006a, b, 2007b) conducted a series of investiga-
construct. A dimensional structure of depression tions examining the latent structure of AS in
was also found in an adult sample in the same youth samples. The results of these studies were
year and more recently in a sample of youth aged consistently interpreted as indicative of
t axonicity, and the researchers were able to repli- Anxiety Disorders

cate these findings in a sample of North American
college students (Bernstein et al., 2007a). Of Generalized Anxiety Two studies have exam-
note, other researchers have been unable to repli- ined the taxonomy of GAD. In the first, responses
cate the taxonic findings of the Bernstein studies. collected from 1175 treatment-seeking adults on
For example, Broman-Fulks et al. (2008, 2010) measures of worry (PSWQ-A) and generalized
conducted a series of taxometric analyses of AS anxiety (GAD-7) were analyzed using multiple
across several adult samples, the results of which taxometric procedures (Kertz et al., 2014). In the
consistently supported a dimensional solution. second, responses to a diagnostic interview for
Similarly, Asmundson et al. (2011) reported evi- GAD administered at two time points to a sample
dence of dimensional AS structure across under- of more than 2000 adults ages 25–74 were con-
graduate and community samples. verted into seven indicators matching DSM-IV
One potential explanation for these discrepant diagnostic criteria for GAD (Marcus et al., 2014).
findings is improvements in taxometric method Notably, all members of this sample endorsed
technology over the years. As Haslam et al. “excessive worry” as a prerequisite for inclusion
(2012) note, the vast majority of taxonic findings in the study, so this variable was not represented
generated through taxometric analysis were pro- as an indicator. In both studies, results supported
duced prior to the introduction and adoption of dimensional models of GAD. In Kertz et al.
the CCFI by Ruscio (2007), and nearly every (2014), clinical interviews administered prior to
taxometric study conducted since this time has admission into the treatment program suggested
found better fit for dimensional models of anxi- that 34% of the sample met diagnostic criteria for
ety disorders and related constructs than categor- GAD, while Marcus et al. (2014) estimated a
ical models (Haslam et al., 2020). All in all, base rate for GAD of 19.5–21.3% in their sam-
reviews of taxometric findings across time sug- ple. However, their taxometric findings suggest
gest that there is little evidence to support the that such designations may be arbitrary.
existence of categories within the vast majority
of psychopathological and personality-related
constructs, including child and adolescent anxi- Health Anxiety Ferguson (2009) applied taxo-
ety disorders. However, other inferences made metric procedures to six indicators of health anx-
from studies of adult anxiety disorders and their iety obtained from a sample of 501 working
risk factors may better inform hypothesis sur- adults. Findings supported a dimensional model
rounding the structures of child anxiety disorders of health anxiety across three taxometric proce-
that have yet to be studied. dures. Notably, the sample only included adults
who reported that they were not being currently
treated for an illness or receiving outpatient care.
Taxometric Findings for Adults These “healthy” adults may not have adequately
represented the full range of health anxiety symp-
Taxometric research has yielded consistent evi- tomatology enough for a taxon within the group
dence for the dimensionality of adult anxiety to have been identified. Also, the indicators used
disorders and their risk factors. We will briefly may not have been representative of the health
summarize the taxometric literature on adult anxiety construct. In response to these limita-
anxiety disorders, bearing in mind the limitations, Longley et al. (2010) continued the investi-
tions that exist for our ability to draw confident gation with a sample of 1083 undergraduate
conclusions from earlier works. CCFIs are adults, though participants were not excluded
reported when applicable in Table 7.1. Finally, based on health status as they had been in
we will discuss the applicability of these adult Ferguson (2009). Four indicators were selected
studies to younger populations at the end of the from three measures of health anxiety that had
section. been administered to the sample and factor
Table 7.1 Taxometric findings for anxiety disorders by sample age

Avg. Sample Avg.
Construct Study Age CCFI Model Supported
Mixed Anxiety Depression Schmidt et al. (2007) 16.6 N/A Categorical
Post-Traumatic Stress Broman-Fulks et al. (2009) 14.6 0.22 Dimensional
Generalized Anxiety Kertz et al. (2014) 35.0 0.32 Dimensional
Marcus et al. (2014) 42.9 0.37 Dimensional
Health Anxiety Ferguson (2009) 40.3 0.39 Dimensional
Longley et al. (2010) 20.8 0.33 Dimensional
Social Anxiety Kollman et al. (2006) 33.0 N/A Dimensional
Crome et al. (2010) N/A (18+) 0.34 Dimensional
Ruscio (2010) 42.4 0.23 Dimensional
Boyers et al. (2017) 19.2 0.38 Dimensional
Weeks et al. (2010) 21.3–33.6 0.66 Categorical
Agoraphobia Slade and Grisham (2009) 33.1 0.24 Dimensional
Separation Anxiety Silove et al. (2007) 37.0 N/A Dimensional
Obsessive Compulsive Olatunji et al. (2008) 19.0 0.35 Dimensional
Symptoms
Worry Ruscio et al. (2001) 18.7 N/A Dimensional
Olatunji et al. (2010) 20.2–33.5 0.31 Dimensional
Somatization Thomas and Locke (2010) 43.0 0.34 Dimensional
Jasper et al. (2012) 22.2–44.4 0.30 Dimensional
Kliem et al. (2014) 47.8–49.3 0.38 Dimensional
Alexithymia Parker et al. (2008) 20.0–35.5 0.32 Dimensional
Mattila et al. (2010) 51.7 0.41 Dimensional
Fear of Pain Asmundson et al. (2007) 39.8 N/A Dimensional
Fear of Evaluation Weeks et al. (2009) 19.0 0.28 Dimensional
Neuroticism Longley et al. (2017) 20.7–62.0 0.31 Dimensional
Intolerance of Uncertainty Carleton et al. (2012) 27.9–36.4 0.28 Dimensional
Disgust Sensitivity Olatunji and Broman-Fulks 19.3–20.7 N/A Dimensional
(2007)
Perfectionism Broman-Fulks et al. (2008) 18.9–19.0 0.37 Dimensional
Note: CCFI scores greater than 0.55 indicated better fit with categorical models, while scores less than 0.45 indicate
better fit with dimensional models. Reported CCFI scores are averaged across all procedures and samples, when appli-
cable. Average age of participants in each sample is reported in years and provided in ranges for studies reporting
multiple samples
analyzed. Taxometric procedures using these ing for symptoms of social anxiety. Five indica-
indicators provided additional support for the tors compiled from a battery of anxiety measures
dimensional latent structure of health anxiety that were chosen to represent the SAD construct in
had been previously identified. subsequent taxometric analyses. The authors
reported that the taxometric plots generated from
their data more closely resembled simulated
Social Anxiety The first taxometric study of the graphs of dimensional structure, and fit indices
structure of SAD used data from a sample of supported their conclusions across three out of
2035 adult outpatients at an anxiety treatment three procedures. Extending this research, both
center (Kollman et al., 2006). Of this group, 471 Crome et al. (2010) and Ruscio et al. (2010)
met criteria for a primary diagnosis of social pho- found evidence for the dimensionality of SAD in
bia (now classified as SAD), though nearly twice large national samples of adults from Australia
this number of outpatients within the sample and the USA, respectively. Finally, Boyers et al.
scored in the upper half of a clinical severity rat- (2017) investigated whether the “performance
only” specifier for SAD represents a discrete sub- Separation Anxiety Though typically seen in
type of fear categorically different from other early childhood, separation anxiety can be
social fears as implied in the DSM-V. From a observed in both child and adult populations
sample of 2019 nonclinical participants, taxo- (Bögels et al., 2013). Taxometric studies of sepa-
metric analyses of indicators for SAD and the ration anxiety in children have yet to be pub-
“performance only” specifier failed to identify lished, but one study has been conducted on a
categorical structure in either construct. sample of 870 adult outpatients at an anxiety
clinical in Australia (Silove et al., 2007). Two
Uniquely, Weeks et al. (2010) performed taxo- taxometric procedures generated plots suggestive
metric analyses on data obtained from a com- of a latent dimensional structure out of indicators
bined sample of community/undergraduate and derived from an adult separation anxiety scale.
clinical populations and identified a taxonic The 15% of the sample that was diagnosed by
structure in SAD. This is the only taxometric clinicians as having separation anxiety prior to
study of anxiety disorders (of which we are the study was not identified in these structural
aware) that generated non-redundant support for analyses, suggesting that whatever diagnostic cri-
a categorical model of an anxiety disorder since teria were being used at the time may have been
taxometric methods were improved by Ruscio arbitrarily segregating anxiety symptoms based
(2007). However, this finding is likely due to the on their perceived domain (i.e., separation from
nature of the combined sample used in this study. an attachment figure). While these findings say
By pre-selecting hypothetical taxonic and non- little about the structure of anxiety more broadly,
taxonic groups for representation within their they suggest that specific manifestations of anxi-
sample based on existing categorical diagnostic ety (e.g., separation anxiety, social anxiety, health
criteria, Weeks et al. (2010) may have influenced anxiety, etc.) may be categorically indistinguish-
the ability of the taxometric procedure to identify able from one another on the basis of domain
true latent classes within the data. This approach alone.
artificially skews results towards distinguishing
not the underlying structure of the construct of
interest, but the structure of the predefined groups Obsessive Compulsive Disorder Though no
that are purported to represent it (Schmidt et al., longer classified as an anxiety disorder in the
2004). DSM-5, obsessive-compulsive disorder (OCD)
shares much of its symptomatology with anxiety
Agoraphobia Only one taxometric study of disorders (Stein et al., 2010). Only one taxomet-
agoraphobia has been conducted with adults. ric study has been conducted on OC symptoms in
Slade and Grisham (2009) analyzed agoraphobia adults. Olatunji et al. (2008) investigated the
survey data from separate samples of clinical structure of OC symptoms in a large sample of
and non-clinical adult populations and found young adult undergraduates. Using two measures
evidence for the dimensional model of agora- of OC symptoms, multiple sets of indicators were
phobia in both. Though unlikely, the separation created for primary symptoms (i.e., obsessing,
of clinical and non-clinical samples in this study ordering, hoarding, perfectionism, etc.) and sub-
leaves open the possibility that agoraphobia may jected to two taxometric procedures. Though
exhibit a dimensional bimodal structure (i.e., some of the results were ambiguous, the majority
two categories, each with a dimensional struc- suggested that OC symptoms endorsed a dimen-
ture). Similar to the aforementioned problem of sional structure. Hoarding was the only exception
combining pre-classified samples for taxometric to this pattern, with its indicators demonstrating
analysis, this limitation can be addressed by an ambiguous-leaning-categorical mean CCFI of
avoiding the a priori categorization of sample 0.54. More recent taxometric research found
constituents. dimensionality in hoarding when analyzing data
from three large samples of community and of somatization in both student samples and the
young adult populations (Timpano et al., 2013). primary care sample, respectively. These findings
Perhaps, the deviancy observed with hoarding were later replicated in two additional samples of
symptoms in Olatunji et al. (2008) was an artifact the German adult population using indicators
of the number of analyses that were run in that taken from alternative measures of somatization
study (nine series in total) or of the indicators (Kliem et al., 2014). Of note, participants in both
used. In any case, research seems to suggest that samples of the Kleim et al. (2014) study ranged
OCD, like other anxiety disorders, is best con- in age from 14 to 92, meaning that these findings
ceptualized as a dimensional construct. are partially representative of the latent structure
of somatization in adolescents as well as adults.
Symptoms
Alexithymia Alexithymia, or the inability to
Worry As mentioned previously, Kertz et al. label or identify with emotions, is associated with
(2014) found evidence supporting a dimensional anxiety in both adults and adolescents (Paniccia
structure of worry in a sample of 1175 adults et al., 2017). Parker et al. (2008) compiled scores
seeking treatment for anxiety. Two previous stud- from community, undergraduate, and outpatient
ies have also looked at the structure of worry in samples from a measure of alexithymia into three
adult populations. In one, scores from 1588 taxometric indicators. Analyses revealed that
undergraduate students on two measures of worry across three samples and three taxometric proce-
were used to create sets of paired, unpaired, and dures, alexithymia was expressed dimensionally
dichotomous indicators, which were then sub- in these populations. In an attempt to generalize
jected to taxometric analysis (Ruscio et al., the findings of Parker et al. (2008), other research-
2001). Three sets of indicators input into two ers extended the taxometric analysis of alexi-
nonredundant taxometric procedures provided thymia to a large sample of Finnish adults
strong evidence for the dimensional structure of (Mattila et al., 2010). A dimensional latent struc-
worry. More recently, Olatunji et al. (2010) repli- ture was supported in both the total sample
cated these findings of dimensionality in two (n = 5194) and subsamples of men and women
adult samples from community and undergradu- therein.
ate populations.
Fear Fear is a key characteristic of anxiety dis-

Somatization Similar to many of the constructs orders, and the identification of taxonic levels of
that we have reviewed thus far, research suggests fear would significantly inform how such disor-
that somatization, the expression of psychologi- ders are treated. Though taxometric studies of
cal distress as physical concerns, is dimension- fear symptoms are sparse, they corroborate much
ally structured. During the course of constructing of what has already been seen with regard to the
a somatization scale, Thomas and Locke (2010) latent structure of anxiety symptoms. The fear of
identified patterns of dimensionality within pain was assessed in 650 treatment-seeking adult
somatic complaints reported by a sample of patients with a measure of pain anxiety symp-
adults experiencing both epileptic and non- toms (Asmundson et al., 2007). This measure
epileptic seizures. Jasper et al. (2012) extended was factorized into four item-parcel (grouped)
this line of research to undergraduate and pri- indicators representing different aspects of pain
mary care samples of German adults, using indi- anxiety and passed through three taxometric pro-
cators derived from a measure of somatic cedures. All three procedures yielded results that
symptom reporting in three taxometric analyses were interpreted as supporting the dimensionality
of the somatization construct. Three taxometric of the fear of pain. Similar findings were reported
procedures evidenced the dimensional structure for the fear of negative and positive evaluations
using a sample of 976 undergraduates (Weeks Perfectionism Considered to be a risk factor for
et al., 2009). These analyses used indicators that a wide range of psychopathologies, perfection-
were formed from multiple measures and pro- ism is an ideal candidate for taxometric analysis.
duced evidence supporting dimensional models Broman-Fulks et al. (2008) administered three
of fears of both negative and positive measures of perfectionism to two large under-
evaluations. graduate samples to test for the existence of a
“perfectionist” taxon within the general popula-
tion. One indicator set from each of the three
Risk Factors measures was created and subjected to four taxo-
metric procedures. On average, results from both
Neuroticism Neuroticism, or the trait-like ten- samples converged on dimensional models of
dency to experience negative affect, is thought to perfectionism.
emerge in childhood and stabilize over the course
of adolescence (Lamb et al., 2002), during which
time it becomes predictive of the development of Discussion
anxiety disorders in late adolescence (Zinbarg
et al., 2016). Longley et al. (2017) conducted A review of the taxometric research among adult
taxometric analyses on data collected from three samples appears to provide strong and consistent
different measures of neuroticism administered evidence that anxiety disorders manifest as
to three large non-clinical undergraduate and dimensional phenomena that are arbitrarily
adult community samples. Indicators of neuroti- dichotomized to create the commonly known
cism from each of these measures consistently diagnostic categories. Similarly, studies indicate
supported dimensional models of the construct. that most anxiety-related vulnerability factors
and symptoms of anxiety disorders that have
been examined via taxometric methodology also
Intolerance of Uncertainty Carleton et al. appear to represent latent continua. Unfortunately,
(2012) are the only researchers to date that have despite expansive evidence for the dimensional-
examined the taxometric structure of intolerance ity of anxiety disorders in adult populations, rela-
of uncertainty (IU), a construct suggested to be a tively little taxometric research has been
risk factor for disorders characterized by exces- conducted with child and adolescent samples.
sive future-oriented concerns (i.e., anxiety disor- Taxometric studies conducted more than a decade
ders, OCD). In this study, both community and ago by Schmidt et al. (2007) and Broman-Fulks
clinical adult subsamples completed a measure of et al. (2009) resulted in contradictory claims
IU. Indicators derived from this measure pro- regarding the latent structure of child and adoles-
duced evidence in support of the dimensional cent anxiety disorders, and the debate has been
latent structure of IU. left relatively uninformed since.
Though the field of clinical psychology has
largely migrated from categorical models of psy-
Disgust Sensitivity Olatunji and Broman-Fulks chopathology to dimensional models in recent
(2007) performed taxometric analyses of scores years, there are several reasons taxometric
reported by two large undergraduate samples on research continues to be needed to ensure that the
two measures of disgust sensitivity. All three pro- dimensional solutions found among adult popu-
cedures used to test the data produced plots sug- lations extend to earlier developmental stages.
gestive of dimensional structure for both One such argument against the invariance of the
samples. latent structures of anxiety disorders across time
is that fear conditioned by an aversive stimulus Conclusion and Future Directions

can generalize to broader stimulus classes over
time (Dunsmoor & Paz, 2015). For example, a Available taxometric evidence robustly supports
child who develops a fear of balloons in response dimensional models of adult anxiety disorders
to an unexpected and aversive auditory stimulus (Haslam et al., 2020), but comparable studies of
may generalize this response over time to other child and adolescent populations are equivocal
stimuli associated with balloons (e.g., birthday and lacking. It is likely that the experiences of
parties), each eliciting fear responses of differing younger populations suffering from anxiety also
intensities and controlling the behavior of the vary in degree, not type, but in the absence of
child in different ways. The presentation of what empirical support for this claim, researchers and
could be diagnosed as a specific phobia in child- clinicians should be wary of the costs and bene-
hood may therefore evolve from basic physiolog- fits associated with assuming either dimensional
ical and behavioral responses (e.g., sympathetic or categorical models of anxiety disorders in
arousal, crying, and avoidance) that appear cate- these populations. Categorical models provide
gorically structured to increasingly complex and clinical utility by allowing clinicians and
contextually controlled behavioral repertoires researchers to more easily discuss and label clus-
(e.g., rituals) that collectively exhibit a dimen- ters of related experiences (i.e., symptoms) as
sional latent structure. However, this argument disorders. By grouping together individuals with
assumes that our capacity for fear generalization shared experiences into “clinical” and “non-
increases over the course of development. clinical” groups, researchers can more conve-
Evidence suggests the opposite is true: compared niently and efficiently compare symptomology
to adolescents and adults, younger children dis- between groups, identify patterns in symptom
play greater rates of fear generalization because development across time within groups, and track
they are less capable of discriminating between changes in group membership throughout the
danger and safety cues in the environment (Glenn course of intervention trials. This sort of approach
et al., 2012; Schiele et al., 2016). Further research is useful to the degree that differences between
is needed to test the more general assumption of putative groups are captured accurately and in
temporal invariance of the latent structures of concordance with the “true” nature of the con-
anxiety disorders. struct of interest. However, when inaccurately
It is also possible that the anxiety disorder drawn, lines dividing those with and without anx-
constructs being measured in youth and adult iety disorders can lead to unequal treatment
populations are separate forms of a broader class availability for individuals straddling the
of pathology, each with independent latent struc- threshold.
tures. Testing this hypothesis would not only As our technologies and methods have
require a replication of extant taxometric studies advanced, we have become increasingly capable
on child and adolescent populations, but addi- of modeling anxiety disorders dimensionally.
tional efforts to clarify how and when childhood Dimensional models preserve valuable informa-
anxiety disorders transition to (or are replaced tion about the nature and presentation of anxiety-
by) their adult variants. Such an argument pre- related suffering that might otherwise be lost in
supposes meaningful differences between adult categorical models; whereas the continuous data
and youth classes of psychopathology as well as associated with dimensional models can be
between the putative pathological and non- divided into groups as needed, the reverse pro-
pathological classes typically tested by taxomet- cess is not possible for categorical data. Another
ric analyses. As such, it would require additional benefit of dimensional models is that they tend to
methodological tools and techniques beyond predict impairment attributable to emotional dis-
those currently available to address. orders (i.e., anxiety and depression) better than
categorical models (Bjelland et al., 2009). In
adults, issues like high rates of comorbidity and
low diagnostic reliability challenge the utility of Bernstein, A., Zvolensky, M. J., Kotov, R., Arrindell,
W. A., Taylor, S., Sandin, B., et al. (2006a). Taxonicity
the DSM’s categorical diagnostic system of anxiety sensitivity: A multinational analysis.
(Kraemer, 2007). However, even though some of Journal of Anxiety Disorders, 20, 1–20.
these criticisms of models of adult of anxiety dis- Bernstein, A., Zvolensky, M. J., Stewart, S. H., Comeau,
orders are supported by comparable evidence M. N., & Leen-Feldner, E. W. (2006b). Anxiety
sensitivity taxonicity across gender among youth.
from child and adolescent populations (e.g., Behaviour Research and Therapy, 44, 679–698.
Schniering et al., 2000), it should not be assumed Bernstein, A., Zvolensky, M. J., Norton, P. J., Schmidt,
that the models themselves are equivalent across N. B., Taylor, S., Forsyth, J. P., et al. (2007a).
developmental periods. Until researchers expand Taxometric and factor analytic models of anxiety
sensitivity: Integrating approaches to latent structural
the taxometric evidence base, these sorts of con- research. Psychological Assessment, 19(1), 74–87.
siderations must be considered when determining https://doi.org/10.1037/1040-3590.19.1.74
how best to assess, measure, and intervene in Bernstein, A., Zvolensky, M. J., Stewart, S., & Comeau,
child and adolescent anxiety disorders. N. (2007b). Taxometric and factor analytic models
of anxiety sensitivity among youth: Exploring the
latent structure of anxiety psychopathology vulner-
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Dimensional Diagnosis of Anxiety
in Youth 8
Dean McKay
The diagnosis of anxiety disorders in children SM-5-TR Diagnostic Categories

D
and adolescents is associated with several prob- of Anxiety Disorders
lems including high comorbidity and low clinical
utility of diagnostic categories. This chapter will Currently, the diagnostic categories for anxiety
begin by outlining the weaknesses of the current disorders are rationally derived and approved by
categorical diagnostic system and reviewing the expert consensus in committee. That is, they are
history and evidence for taking a dimensional grouped together according to phenotypically
approach to the diagnosis of anxiety disorders in similar symptoms. This is in contrast with other
children and adolescents. The problem of the taxonomic models, such as the Linnaean hierar-
high comorbidity of anxiety and depression in chical frameworks that define categories through
youth will be discussed, followed by a review of conceptual signs and indicators (discussed in de
several quantitative structural models which have Queiroz & Good, 1997). However, the tradition
been proposed to differentiate between the shared in psychology is to evaluate dimensionally, as
and specific components of anxiety and depres- evidenced by the types of measures used to assess
sion. Based on the research indicating that anxi- symptom severity. There is a growing movement
ety disorders are best classified as highly within psychology to classify using the hierarchi-
correlated symptom clusters comprising internal- cal taxonomy of psychopathology (HiTOP;
izing syndromes, approaches to assessment and Ruggero et al., 2019), but this model has not yet
diagnosis will be covered in the last section of developed sufficiently to apply in youth anxiety
this chapter. Tools that have been validated to disorders. Therefore, there is tension between the
measure anxiety and depression dimensionally in clinically relevant practice of rating symptom
youth will be presented, as well as measurement severity dimensionally and assigning a categori-
of narrow traits that have been found to put chil- cal diagnosis.
dren and adolescents at risk for the development Notably, there were only three categories of
of pathological anxiety. Finally, we will discuss anxiety disorders in the second edition of the
the need to move toward a system of classifica- Diagnostic and Statistical Manual of Mental
tion that corresponds more directly to effective Disorders (DSM-ll; American Psychiatric
interventions for anxiety disorders in youth. Association, 1968). There are nine categories in
the current edition (DSM-5-TR; American
D. McKay (*) Psychiatric Association, 2022). Brown et al.
Department of Psychology, Fordham University, (1998) argued that the increasing number of anxi-
Bronx, NY, USA ety diagnoses indicates that the “classification
https://doi.org/10.1007/978-3-031-14080-8_8
112 D. McKay
systems have become overly precise to the point Since the earlier recommendations that a
that they are now erroneously distinguishing dimensional approach be adopted, a growing
symptoms and disorders that actually reflect effort to develop statistical methodologies for
inconsequential variations of broader, underlying identifying entities that are either continuous or
syndromes” (p. 179). This reflects the “splitting” taxonic has emerged. This approach, referred to
movement, whereby disorders are defined in as taxometric analysis, has allowed for the identi-
increasingly narrow domains. Accordingly, with fication of conditions that may be taxonic (i.e.,
this level of specificity, existing diagnoses can in composed of some discrete point whereby levels
some instances lack syndromal validity and fail of a psychopathological indicator would suggest
to offer distinctions that allow for effective treat- a unique and separate entity) or may be on a con-
ment planning. tinuum of severity. Two notable examples from
the anxiety disorder literature illustrate this. The
first involves dissociation, which is commonly
imensional Approaches: A Brief
D associated with trauma and acute anxiety and has
History been shown to be taxonic. That is, scores on a
major measure of dissociation can be categorized
Dimensional models of psychopathology have where some individuals are considered non-
been advocated for some time now, and the argu- dissociators (or to a very limited degree) and
ments advanced for this approach include several those scoring above that point are considered dis-
important points. First, categorically based diag- sociators (Waller et al., 1996). On the other hand,
nosis assumes that each disorder is a discrete anxiety sensitivity has been examined for taxonic
entity (Carson, 1991). This is generally an inac- status. Anxiety sensitivity refers to the degree
curate view, but it is the one understood by the that changes in internal bodily state are experi-
architects of the symptom-based DSM (Frances enced as dangerous, and it is commonly present
et al., 1991). Second, since diagnoses in the cur- in most anxiety disorders (Taylor, 1999).
rent DSM are formulated based on consensus Research has shown that this construct is non-
agreement in committees and task forces, rather taxonic, or dimensional (Broman-Fulks et al.,
than based on medical and/or psychological eti- 2010).
ology from agreed upon theoretical concepts, the In the case of the major constructs used to
diagnoses are potentially arbitrary entities whose understand anxious psychopathology, the major-
existence is based on a posteriori reasoning (for a ity are dimensional in nature. Among those that
discussion of different taxonomic methods and are dimensional in nature are worry (Olatunji
models, see Blashfield et al., 2009). Third, et al., 2010), posttraumatic reactions (Ruscio
dimensional models permeate other medical sci- et al., 2002), and obsessive-compulsive symp-
ences, where severity and complicating factors toms and beliefs (Haslam et al., 2005). Likewise
play a prominent role in classification. These fac- in children, there is a high degree of dimensional-
tors are critical in any taxonomy because they ity evident in anxiety disorder relevant constructs.
contribute to prediction of course and treatment Notably, anxiety sensitivity (Bernstein et al.,
outcome (again, see Blashfield, Keely, & 2007) and trauma (Goodman et al., 2003) both
Burgess). Finally, a guiding principle in the have been found to have a dimensional structure.
development of many categories in the current There have been far fewer taxometric studies
DSM was the degree that clinicians would be involving children, likely due to the large sample
likely to accept the diagnosis and thereby utilize sizes necessary for stable estimates of effect (see
it in evaluating clients (Carson, 1991). This last Waller & Meehl, 2002, for a technical discussion
difficulty is perhaps most problematic since it of taxometric analysis).
undermines the very utility of a diagnostic sys- What this suggests is that most psychological
tem by formulating diagnosis on the basis of con- indicators involved in conceptualization and
sensus rather than syndromal validity. assessment of anxiety disorders have a
8 Dimensional Diagnosis of Anxiety in Youth 113
d imensional quality. This would rule out a cate- other methods of assessing these constructs, indi-
gorical approach since such models eliminate a cating that this is not due to common method
great deal of information regarding symptom variance.
severity and relevant treatment components. Among youth, there is significant amount of
overlap between symptoms of anxiety and
depression. In particular, Brady and Kendall
The Problem of Comorbidity (1992) found that the correlation between self-
report measures of anxiety and depression ranged
From an epidemiological perspective, the current from r = 0.50 to r = 0.70 among children and
DSM system has resulted in a high probability of adolescents. Although this high correlation may
comorbid conditions. Brady and Kendall (1992) be due in part to similar item content on self-
reported a 16% comorbidity rate in a community report measures of anxiety and depression, previ-
sample of children and adolescents that were not ous research has found that there is still substantial
seeking treatment and comorbidity rates ranging correlation when overlapping items are removed
from 28% to 62% in clinical samples of youth (Stark & Laurent, 2001; Cole et al., 1997).
that were seeking treatment. As was discussed Generally, the net result has been to recognize
above concerning the problem of dimensional that each is dimensional, rather than discrete enti-
versus discrete categories, the problem of comor- ties, given the robustness of such a finding. Some
bidity rate has been addressed in the literature. in the psychiatry profession have called for a
For example, Mineka (1998) described “exces- purely dimensional approach given that (a)
sive diagnostic splitting” as a potential cause of depression and anxiety are commonly experi-
comorbidity with regard to highly similar disor- enced in the general population and (b) severity is
ders (e.g., overanxious disorder and GAD in chil- not tied to a reliable biological substrate
dren; Caron & Rutter, 1991). Researchers have (Goldberg, 2000). Indeed, consider that, even in
also provided excellent suggestions for handling the realm of behavioral genetics where the aim is
this issue in conceptualization and treatment to identify phenotypic signs of psychiatric distur-
planning. For example, Rachman (1991) offered bance, the field relies on dimensional models
four recommendations for handling comorbidity, (Kendler, 2006). This is largely because there is
including (a) behavioral analysis of presenting recognition of the range of disturbance present in
symptoms, (b) assessment of subjective experi- individuals suffering from psychiatric problems,
ence of all comorbid conditions to identify over- and the dimensional approach permits greater
lapping features, (c) commonalities in reliability in findings given the increased vari-
psychophysiological responses, and (d) semantic ability and hence greater power in statistical tests
overlap among diagnoses. (DiLalla, 2004).
Around this same time, it was widely recog- Given the reliance on categorical diagnoses,
nized that depression and anxiety tend to co- and the concordant allegiance to specific levels of
occur, or exist together at sub-threshold levels, analyses (i.e., biomedical, psychosocial), it has
but collectively lead to serious psychological dis- been suggested that all mental health profession-
turbance (Barlow & Campbell, 2000). This als exert caution in conceptualization. To ensure
emerged due to the frequent finding that, regard- greater consideration for the full range of puta-
less of sample, depression and anxiety tend to tive dimensional variables that may impinge on
correlate. In the case of self-report measures, the presenting mental health symptoms, Kendler
correlation between depression anxiety is typi- (2012) has called for a pluralistic approach to the
cally greater than 0.6, even after removing items assessing psychiatric conditions. This means that
that could reasonably reflect the other construct every level of analysis be considered in under-
and thereby inflate the correlation (Barlow, standing a case, from the biological underpin-
1991). Similar results have been observed for nings up through sociocultural influences.
114 D. McKay
Alternate Conceptualizations was negatively correlated with both depression

of Anxiety Disorders symptoms (r = −0.50, p < 0.001) and anxiety
symptoms (r = −0.34, p < 0.001). Although these
Because of the high level of comorbidity, it has initial results seemed to refute the specific rela-
been suggested that a quantitative approach to tionship of PA to depression symptoms, Crook
diagnosis be used to uncover actual, rather than and colleagues also performed hierarchical
perceived, similarities among mood disorder regression to examine the partial correlations of
diagnoses. Several models have been proposed in PA and NA with measures of anxiety and depres-
which correlated syndromes are grouped together sion, and they found that PA had a significant
in the same diagnostic class. These models aim to negative partial correlation with depression
explain the shared and specific factors contribut- scores when anxiety and NA scores were con-
ing to the etiology of anxiety and depression and trolled, whereas PA was unrelated to anxiety
serve to identify relevant treatment targets. scores when depression and NA scores were
controlled.
Negative Affect and Positive Affect Negative
affect (NA) is the tendency to experience negative Tripartite Model Clark and Watson (1991)
moods (e.g., sadness, fear, guilt, and hostility) and expanded upon the original two-factor model of
has been described as a stable trait. It has been anxiety and depression by introducing another
proposed that NA should be considered a main factor. They proposed the tripartite model as a
vulnerability factor for the development of anxi- means of differentiating anxiety and depression
ety and depression (Clark, Watson, & Mineka, despite their high symptom overlap and diagnos-
1994). Positive affect (PA), on the other hand, has tic comorbidity, which posits that depression and
been suggested as a vulnerability factor specifi- anxiety both share the common component of
cally related to depression. Watson, Clark, and NA. Depression, however, is specifically charac-
Tellegen (1988b) described PA as reflecting “the terized by low PA, whereas anxiety is associated
extent to which a person feels enthusiastic, active, with high physiological hyperarousal (PH).
and alert” (p. 1063), with low PA reflecting anhe- While NA and PA have been described as stable
donia. Watson & Tellegen (1985) theorized that temperaments or personality traits, PH has not.
these personality dimensions could be used to dif- However, Watson et al. (1995a, b) have related
ferentiate between anxiety and depression. the concept of PH to anxiety sensitivity (AS), and
Specifically, he hypothesized that NA is a non- AS has been described in the literature as a trait
specific factor related to both anxiety and depres- that is a risk factor for the development of anxiety
sion and that the existing symptom overlap and disorders (McNally, 1990).
resulting comorbidity are due to this shared trait.
Furthermore, he suggested that PA is a specific Barlow et al. (1996) have also described a
factor that could be used to distinguish between very similar three-factor model for conceptualiz-
anxiety and depression because they found that ing anxiety and depression which attributes the
PA was related (negatively) to depression diagno- development of these disorders to problems with
ses in adults, but PA was not correlated with anxi-
three basic emotions: anxiety (or anxious appre-
ety disorders (Watson, Clark, & Carey, 1988a). hension), fear, and depression. Their model indi-
cates that (a) general distress (i.e., high NA) leads
Among a non-clinical sample of elementary to anxiety (anxious apprehension), (b) autonomic
school-aged children, Crook et al. (1998) did not arousal leads to fear/panic, and (c) anhedonia
find support for this model. Rather, they found (i.e., low PA) and hopelessness lead to depres-
that NA was significantly related to both self- sion. As in the tripartite model, autonomic arousal
reported depression symptoms (r = 0.66, is theorized to be specific to anxiety diagnoses,
p < 0.001) and self-reported anxiety symptoms while anhedonia/low PA is related only to
(r = 0.68, p < 0.001). They also found that PA depression. High NA/distress is hypothesized to
be a common factor to both anxiety and and social phobia. When PA was added to the
depression. structural models, there was a significant nega-
Although the tripartite model was developed tive path from PA to depression. Notably, after
to explain the relationship between anxiety and creating a path from PA to depression, the modi-
depression in adults, it has been shown to be rel- fication indices suggested that a path should also
evant to children and adolescents as well. For be added from PA to social phobia. A significant
example, in a large sample of anxious and negative path was found between PA and social
depressed youth, Lerner et al. (1999) found fac- phobia, and the results indicated that the fit of this
tors from measures of anxiety and depression model was so good that it would not be improved
that corresponded to the models described in by adding additional paths from PA to any other
Clark and Watson (1991). Furthermore, in a large latent variable (i.e., other DSM-IV anxiety diag-
unselected sample (N = 1289) of children, similar noses). Furthermore, the strength of the path
findings were obtained using a different assess- between PA and depression (−0.29) was compa-
ment of depression and anxiety and were repli- rable to the strength of the path from PA to social
cated in a smaller second sample (N = 300) phobia (−0.28). Finally, the addition of PH to the
(Chorpita, Plummer, & Moffit, 2000). The rela- structural models did not improve the fit of the
tionship among NA, PA, and PH was further models. In terms of the different anxiety disor-
examined among inpatient children and adoles- ders, the strongest path from PH was found to
cents, and support was again found for the tripar- panic disorder/agoraphobia. The paths from
tite model among youth (Joiner & Lonigan, OCD and social phobia to PH were not signifi-
2000). Although many studies have supported the cant. Notably, the path from GAD to PH was sig-
tripartite model, there is some evidence that the nificant and negative.
relationship among the three variables (i.e., NA, Turner and Barrett (2003) found that the tri-
PA, and PH) may not be identical across all of the partite model was consistent across three age
anxiety disorder diagnoses. In particular, there is groups (ages 8–9, 11–12, and 14–15) suggesting
evidence that predictions made using the tripar- that the three major components of the model are
tite model do not hold for youth diagnosed with not developmentally dependent. The balance of
social anxiety disorder. research has generally supported the tripartite
Brown et al. (1998) examined the structural model, but much of this has involved self-report
relations among NA, PA, and PH in a large sam- measures or assessments that do not necessary
ple of individuals with one of five DSM-IV diag- pose a strict test of the model (Anderson & Hope,
noses: generalized anxiety disorder (GAD), 2008). However, the tripartite model has shown
depression, panic disorder, obsessive-compulsive considerable promise in assessment of anxiety in
disorder (OCD), and social phobia. The use of youth, may be relatively robust across major anx-
structural equation modeling allowed the iety diagnoses, and illustrates the potential clini-
researchers to test the tripartite model with a cal utility of a dimensional model of nosology.
dimensional approach to the DSM diagnostic cat-
egories as opposed to other approaches that Hierarchical Models Although there has been
would require the researchers to confirm a cate- empirical support for the tripartite model of
gorical diagnosis. Brown and colleagues found depression and anxiety, this structural model
that all paths from NA to the DSM-IV disorder asserts that all anxiety diagnoses are character-
factors were statistically significant, which sup- ized by the shared component of high autonomic
ports the notion that NA is a general dimension arousal, which differentiates anxiety from depres-
common to mood and anxiety disorders. The sion. Researchers have instead proposed that a
strength of the relationship varied across diagno- hierarchical model of anxiety disorders may be
sis, with the strongest relationships existing more appropriate to account for the heterogeneity
between NA and depression and NA and GAD. of anxiety diagnoses (Brown et al., 1998; Zinbarg
The smallest association was found between NA & Barlow, 1996). In this model, each anxiety
116 D. McKay
d isorder has unique and shared components, with comorbidity can be explained by a high correla-
the shard component representing a higher-order tion among the diagnoses in youth.
factor of anxious apprehension (i.e., high NA). The integrative hierarchical model need not be
This model not only accounts for the high corre- confined to anxiety disorders and depression
lation among anxiety disorder diagnoses due to alone, but can be broadened to encompass other
this shared component but also accounts for the disorders that are characterized by high NA
high comorbidity among anxiety and depression (Mineka et al., 1998). Krueger and Piasecki
because high NA is common to depression as (2002) proposed the hierarchical-spectrum
well as anxiety. model, which was an attempt to capture the cor-
relation among DSM diagnoses by clustering
Mineka, Watson, and Clark (1998) suggested symptoms to comprise syndromes with these
a more comprehensive structural model that com- syndromes comprising broader families of disor-
bines the tripartite model with the hierarchical ders or spectra. The broadest categories identified
model described above based on the fact that it is are the internalizing and externalizing disorders,
unlikely that each is equally and adequately with the internalizing disorders being comprised
explained by the dimension of autonomic hyper- of depression and the anxiety disorders.
arousal as proposed by those models. Therefore, Externalizing disorders include substance depen-
Mineka and colleagues proposed the integrative dence, antisocial behavior, and disinhibited
hierarchical model, which suggests that syn- behavior diagnoses. This model has been promis-
dromes have both common and unique compo- ing in understanding anxiety disorders (Taylor
nents. As in previous models, high NA/distress is et al., 2010), but has not yet been extensively
considered to be the shared component of both examined in youth.
anxiety disorders and depression, but anxious Krueger (1999) analyzed data from the
arousal is not viewed as broadly characteristic of National Comorbidity Study (NCS) to find that a
all anxiety disorders. Instead, each individual three-factor structure best accounted for the rela-
anxiety disorder is presumed to have some unique tionship among psychiatric diagnoses. The three
component that differentiates it from all others. latent factors were anxious-misery (which
Anxious arousal is viewed as the specific compo- included major depression, dysthymia, and
nent of panic disorder alone. GAD), fear (which included panic disorder, ago-
Support for this model has been found in chil- raphobia, social phobia, and simple phobia), and
dren using structural equation modeling. In a externalizing disorders (which included alcohol
sample of children, Spence (1997) examined four dependence, drug dependence, and antisocial
models to see which best explained the structure personality disorder). The anxious-misery and
of self-reported anxiety symptom data (i.e., a fear latent factors were highly correlated and thus
single-factor model, a six uncorrelated factor were found to comprise a second-order factor of
model for each specific DSM-IV anxiety diagno- internalizing disorders, which collectively form a
sis, a six correlated factor model, and a higher- group of conditions that tend to co-occur in vary-
order model with six first-order factors loading ing levels. Interestingly, while the three-factor
onto a single second-order factor). The results structure was found for the total NCS sample, in
indicated that the correlated six factor model with a treatment-seeking sample, the lower-order
these six factors loading onto a higher second- latent factors of anxious-misery and fear could
order “anxiety” factor provided the best fit to the not be recovered. This suggests that among indi-
data. Additionally, she found the major propor- viduals experiencing functional impairment the
tion of variance in anxiety symptoms was individual diagnoses are even more highly corre-
explained by this higher-order anxiety factor, lated in a “superclass” of emotional disorders
which suggests that while there are distinguish- (Clark & Watson, 2006; Krueger & Markon,
able anxiety diagnostic categories, the high 2006; Watson, 2005). Since then, the HiTOP
model has been further refined, although these lems, and competencies in children aged 4–18.
analyses have not yet been extended to child The TRF is completed by teachers and is identi-
samples. cal in content to the CBCL. The clinical scales of
The presence of such a superclass of disorders the CBCL and TRF are comprised of a total prob-
provides additional weight to the need for a lems score, internalizing problems, externalizing
dimensional approach to diagnosis since the problems, and eight syndromes (i.e., aggressive
underlying phenotype of anxiety confers a higher behavior, delinquent behavior, withdrawn,
risk for a wide range of putative psychiatric con- somatic complaints, anxious/depressed, attention
ditions. Hereditability data has borne this out, problems, social problems, and thought prob-
whereby no single diagnosis increases the risk lems). These syndrome scales were not devel-
for anxiety disorder in offspring. Instead, the oped to reflect DSM-IV diagnoses, but they were
presence of any anxiety disorder increases the derived through multivariate statistical analyses
risk of any anxiety disorder in offspring (Hettema to identify separate empirically validated syn-
et al., 2001). dromes in line with the hierarchical models
described above. Specifically, with regard to anx-
iety, it was determined that anxiety and depres-
Measuring Anxiety Along sion were so highly correlated they represent a
a Dimension in Children singular syndrome in youth.
Although the CBCL and TRF were originally
In general, the procedures used to assess and developed with this empirically based approach
diagnose anxiety in children and adults are quite to identifying symptoms along a continuum,
similar and typically include diagnostic inter- Achenbach et al. (2003) created DSM scales by
views, self-report measures, and behavioral asking pediatric psychologists and psychiatrists
assessment. However, it is important to consider from diverse cultural backgrounds to rate how
developmental differences throughout the assess- consistent CBCL/TRF items were with a specific
ment process because due to speed of physical, DSM category. Achenbach et al. selected items
emotional, and cognitive development in child- that were reliably rated as “very consistent with
hood, assessment strategies will differ according the DSM category” to create the DSM scales. A
to age. For example, a multi-informant, multi- six-item anxiety subscale was developed through
method approach is recommended to gather com- this approach. Kendall et al. (2007) noted that
prehensive information about symptoms and these six items do not include any somatic symp-
impairment. Thus, in addition to clinical inter- toms, and this omission calls the validity of the
view, observation, and self-report, reports from anxiety subscale into question given that somatic
parents and teachers are recommended when symptoms are a necessary criterion for many of
assessing emotional symptoms in a child, and the the DSM-IV anxiety disorder diagnoses. Thus,
amount of collateral data needed from caretakers Kendall and colleagues derived an alternative
is typically inversely related to the age of the measure of anxiety based on the CBCL/TRF
child. Furthermore, when assessing young peo- items.
ple, it is also necessary to have knowledge of nor- Kendall et al. (2007) developed an initial list
mative development so that manifestations of of 22 items by asking experienced clinicians with
“normal fears” are not considered abnormal a specialty in childhood anxiety disorders to
behaviors (Beidel & Turner, 2005). select CBCL/TRF items related to the diagnosis
The Child Behavior Checklist (CBCL; of an anxiety disorder. Of these items, 18 achieved
Achenbach, 1991; Achenbach et al., 2003) and item-total remainder estimates above 0.40 and
Teacher Report Form (TRF; Achenbach, 1991) were retained in their anxiety scale. These
are the most widely used parent and teacher researchers found that their anxiety scale signifi-
reports. The CBCL is a standardized assessment cantly discriminated anxious and non-anxious
that asks parents to report on behaviors, prob- children aged 9–13, and their anxiety scale better
118 D. McKay
predicted an anxiety disorder diagnosis than did standing difficulty in distinguishing anxiety from
the anxious/depressed and internalizing scales of depression (see, e.g., Rapee & Barlow, 1991).
the CBCL and TRF. In addition, they found that A third measure that has been developed to
their anxiety scale was sensitive to treatment measure mood symptoms along a dimension is
effects. Participants who received treatment dem- the Mood and Anxiety Symptom Questionnaire
onstrated a significantly lower score after treat- (MASQ; Watson et al. (1995a, b). The MASQ
ment, while those on the waitlist showed no was created as a specific measure of the tripartite
significant change in score. Therefore, Kendall model described above. It is a 77-item self-report
et al.’s (2007) anxiety subscale of the CBCL measure with three subscales: (1) General dis-
seems to be a good predictor of pathological anx- tress: depressive symptoms (12 items), anxious
iety in children and adolescents and can be used symptoms (11 items), and mixed symptoms (15
to identify gains made in treatment. However, items), (2) anxiety-specific [anxious arousal
there is some evidence that its utility may depend (AA), 17 items], and (3) depression-specific
on the reporter. Kendall and colleagues found [anhedonic depression (AD), 22 items]. Buckby
that when compared to the CBCL anxiety sub- et al. (2007) found support for the clinical use of
scale developed by Achenbach et al. (2003), their the MASQ to differentiate between anxious and
anxiety scale better predicted anxiety disorder depressed adolescents and young adults. Using
status according to mother report, while the ROC curve analyses, these authors found that the
Achenbach et al. anxiety subscale better pre- AD scale accurately predicted the presence of a
dicted anxiety disorder status according to father mood disorder (72.8%), and the AA scale pre-
report. dicted anxiety disorders (61%). Thus, it seems
Another dimensional measure that may be that the AD scale may be superior to the AA scale
useful for measuring factors related to anxiety is in predicting the presence of the particular disor-
the Positive and Negative Affectivity Scale – der it is intended to measure. Notably, the AA
Child version (PANAS-C; Laurent et al., 1999). scale did better at identifying the absence of an
The PANAS-C is a 20-item self-report measure anxiety disorder (83.5%). Furthermore, Buckby
consisting of two scales: positive affect (PA) and et al. (2007) found that AA and AD scores were
negative affect (NA). Respondents are asked to highly and significantly correlated in all partici-
rate how often within the last week they have pants with a current Axis I disorder (r = 0.59).
experienced 20 mood adjectives. The 10 positive This high correlation calls into question the
mood adjectives and 10 negative mood adjectives assumption that these are separate constructs,
are rated on a 5-point Likert-type scale. The scale which is in line with the hierarchical models
choices are “very slightly or not at all,” “a little,” which indicate that these both fall on the broader
“moderately,” “quite a bit,” and “extremely.” The spectrum of internalizing disorders.
findings suggest that the children’s version of the
PANAS has a similar structure as the adult coun-
terpart. Since the development of this scale, sev- arrow Traits and Risk Factors
N
eral investigations have shown that it performs in Youth
consistently across different cultural groups
(Kiernan et al., 2001), in unselected elementary Given that heredity studies suggest that the pres-
and high school children (Jacques & Mash, ence of an anxiety disorder in a biological parent
2004), and in children with diagnosed anxiety predicts development of any anxiety disorder in
disorders (Hughes & Kendall, 2009). This last offspring (Hettema et al., 2001), it is assumed
study identified difficulties in discriminant valid- that a general tendency to develop anxiety disor-
ity for the scale, however, with higher than antici- ders (i.e., anxiety proneness) is inherited rather
pated relations with social anxiety and depressive than a specific anxiety disorder (Turner et al.,
symptoms. In some ways, this is not surprising 2005). Thus, it is recommended that assessment
and reflective of the aforementioned long- also includes attention to these personality traits
and temperaments that have been identified as anxiety sensitivity have been described as having
risk factors for the development of anxiety the “fear of anxiety” (Reiss et al., 1988, p. 341).
disorders.
AS has consistently been shown to be higher
Behavioral Inhibition Behavioral inhibition among youth with anxiety disorders as compared
(BI) is a temperamental trait that is character- to those without anxiety (Hayward et al., 1997;
ized by the tendency of children and adolescents Weems et al., 2002). This indicates that AS likely
to become uncomfortable in, and avoid, novel serves as a risk factor in the development and
social situations. These youth are extremely shy maintenance of anxiety disorders in young peo-
and are reluctant to engage in adventurous activ- ple. AS is measured using the Childhood Anxiety
ities or participate in unfamiliar social situations Sensitivity Index (CASI; Silverman et al., 1991).
(Kagan et al., 1988). BI has consistently been
found to be related to the development of anxi- Anxiety Control Anxiety control (AC) is a cog-
ety disorders, particularly social anxiety disor- nitive construct that is defined as a person’s per-
der (Hirschfeld- Becker et al., 2006). ceived control over his or her emotional and
Furthermore, BI seems to be most predictive of bodily reactions due to anxiety (e.g., internal
anxiety disorders when it is found among the physiological reactions) as well as his or her per-
children of parents with anxiety disorders ceived control over external events or threats that
(Biederman et al., 2001). cause anxiety (Rapee et al., 1996). Low AC has
been identified as a factor that can differentiate
BI is typically measured using objective stan- between youth who have been referred to a clinic
dardized laboratory observation protocols which for anxiety treatment and controls, and AC has
involve exposing toddlers and preschoolers to been shown to predict anxiety disorder status
unfamiliar people and situations. There are also among children and adolescents when control-
several parent, teacher, and self-report measures ling for anxiety symptoms (Weems et al., 2003).
of BI. For example, the Behavioral Inhibition
Questionnaire (BIQ; Bishop et al., 2003) may be The Anxiety Control Questionnaire for
used to assess BI in preschool-aged children (i.e., Children (ACQ-C; Weems et al., 2003) may be
3–5 years old). There are both parent and teacher used to measure AC. The ACQ-C measures
report forms of the BIQ. In older children and beliefs along two dimensions: (1) Internal reac-
adolescents (i.e., 11–18 years old), the Behavioral tions (e.g., “I can take charge and control my
Inhibition Instrument (BII; Muris et al., 1999) feelings”) and (2) external threats (e.g., “When
can be used. something scares me, there is always something I
can do”). In a recent study, Marin et al. (2008)
Anxiety Sensitivity Anxiety sensitivity (AS) found that both dimensions of AC predict anxiety
refers to a person’s beliefs that his or her anxious symptoms in youth, but they found a different
physical symptoms will lead to aversive physical, pattern for boys and girls. Specifically, in boys,
psychological, and social consequences (Reiss, low perceived control over internal reactions pre-
1991; Reiss et al., 1986). In other words, AS can dicted anxiety symptoms. However, in girls, low
be understood as the likelihood for an individual perceived control over external threats predicted
to report that normal bodily changes associated anxiety symptoms.
with anxiety are likely to have extreme negative
consequences. For example, an individual with Diathesis-Stress Model The presence of any
high anxiety sensitivity is likely to believe that one of these identified risk factors alone is likely
heart palpitations are a sign of a heart attack, not sufficient to lead to the development of an
whereas an individual low on anxiety sensitivity anxiety disorder. In other words, even if a child is
perceives heart palpitations to be nothing more anxiety-prone, a disorder’s onset will probably be
than brief physical discomfort. Those with high triggered by the interaction of the biological
120 D. McKay
p redisposition with environmental/psychological anxiety disorder without attention to the identi-

factors (e.g., parenting factors) as described in fied correlate of low positive affect may not be as
the diathesis-stress model. In fact, there is evi- effective, but this relationship that has been
dence that some of these inherited vulnerability shown empirically is not reflected in the diagnos-
factors may be mitigated by environmental fac- tic criteria. Similarly, Marin et al. (2008) found
tors. For example, BI, which has been identified that different aspects of anxiety control were use-
as a relatively stable temperamental trait, has ful for predicting anxiety disorders for boys and
been shown to be reduced among young children girls, which suggests that cognitive behavioral
if parents are instructed in the risks associated interventions may have separate targets for the
with overprotective parenting and how to inten- different genders. As the literature covered in this
tionally expose their child to novel social situa- chapter amply illustrates, there are many advan-
tions (Rapee et al., 2005). There is ample tages that can be conferred on treatment of chil-
empirical support for the usefulness of measuring dren with anxiety disorders by relying on
these narrow traits as part of dimensional diagno- dimensional perspectives. Further research into
sis of anxiety disorders in youth. Because many quantitatively derived models for the dimensional
of these traits are currently measured via self- diagnosis of anxiety in youth promises to inform
report, Turner et al. (2005) recommended that and improve our treatment of these disorders by
physiological reactivity can be used as a measure highlighting the relevant personality traits, cogni-
of anxiety proneness that is not dependent on tive factors, and emotional and behavioral
subjective report. responses that will lead to increased functioning.
This can also provide a rich understanding of
what dimensions may potentially form distinct
Correspondence to Treatment categories at the extreme boundaries based on
Models Rather Than Diagnostic empirically based evaluations. In contrast to the
Categories large and diverse number of diagnoses that cur-
rently exist, it appears that there are in fact
A shift in diagnostic classification from a cate- numerous dimensions but few distinct binary cat-
gorical to dimensional conceptualization can lead egories. Refinement of dimensional models
to a fuller understanding of the components that would permit better treatment decisions based on
underlie anxiety and mood problems. The current severity level and on the rarer categorical psychi-
DSM-IV criteria focus on the differential diagno- atric conditions.
sis of anxiety problems at the risk of neglecting
aspects relevant to the amelioration of these anxi-
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Transdiagnostic Treatment Models
for Child and Adolescent Anxiety 9
Disorders
Ashley R. Karlovich , Elizabeth R. Halliday ,

and Jill Ehrenreich-May
Following from the initial publication of the reliably, if narrowly, defined concerns, particu-
Diagnostic and Statistical Manual of Mental larly with regard to internalizing disorders (Pearl
Disorders (DSM; American Psychiatric & Norton, 2017). However, this “disorder-
Association [APA], 1952), mental health condi- specific” approach to treatment development is
tions were historically conceptualized as distinct arguably poorly suited to youth samples, and
and separable diagnostic categories. These cate- childhood anxiety disorders, in particular.
gories each have specific criteria to classify indi- In the case of anxiety disorders in children and
vidual disorders, in part to ease communication adolescents, comorbidity rates (i.e., the co-
about such concerns and to provide a reliable occurrence of multiple mental health disorders)
means by which to assess change in specific diag- are high (Mohammadi et al., 2020), diagnoses
nostic criteria related to particular disorders over frequently emerge and change during youth
time (Barlow et al., 2004). Following the devel- development (Garber & Weersing, 2010), diag-
opment of the DSM-III (APA, 1980), the ability nostic reliability may be lower than in adults
to reliably classify change in anxiety and other (Norton & Paulus, 2017), and symptom presenta-
disorders was associated with a paradigm shift in tions across disorders may appear quite similar
clinical psychology, during which several, rela- (Leyfer et al., 2013). A growing body of research
tively brief, often cognitive-behavioral interven- on common mechanisms in youth anxiety and
tions were developed to ameliorate these now depressive disorders (e.g., high negative affect,
intolerance of uncertainty, etc.) has subsequently
guided the development and empirical testing of
Ms. Karlovich and Ms. Halliday have no known conflict
more transdiagnostic or multidiagnostic
of interest to disclose. Dr. Jill Ehrenreich-May is the first
author of the therapist guide and workbooks for the evidence- based therapies to treat children and
Unified Protocols for Transdiagnostic Treatment of adolescents with co-occurring anxiety disorders
Emotional Disorders in Children and Adolescents (UP-C and other related emotional disorders (e.g.,
and UP-A) and receives a royalty from these publications.
depressive, externalizing, eating). The need for
Dr. Ehrenreich-May (also) receives payments for UP-C
and UP-A clinical trainings, consultation, and implemen- transdiagnostic interventions is bolstered by their
tation support services. flexible treatment structure, which allows for
A. R. Karlovich · E. R. Halliday
J. Ehrenreich-May (*)
Department of Psychology, University of Miami,
Coral Gables, FL, USA
e-mail: j.ehrenreich@miami.edu
https://doi.org/10.1007/978-3-031-14080-8_9
126 A. R. Karlovich et al.
easier adaptation to variability in case presenta- presence of an anxiety disorder increases the risk
tion (Ehrenreich-May & Chu, 2013) and poten- of having or developing another anxiety disorder
tially speeds dissemination efforts (McHugh later in childhood (Bittner et al., 2007; Garber &
et al., 2009). Weersing, 2010). These sequential and concur-
rent comorbidity patterns may also be driven by
crosscutting processes that contribute to the
Comorbidities development of anxiety disorders (e.g., poor cog-
nitive reappraisal of threat, greater parental
The criteria for most anxiety disorders is charac- accommodation behaviors, etc. (La Buissonnière-
terized by similar features, including persistent Ariza et al., 2018)).
fear or anxiety in a number of domains (or a more The co-occurrence patterns of anxiety and
singular one, as in the case of panic disorder or a depression and youth are also important for inter-
specific phobia), behavioral responses to such vention given the high prevalence of these con-
fears or anxiety (e.g., avoidance, escape behav- cerns (Garber & Weersing, 2010; Leyfer et al.,
iors) that temporarily suppress distress related to 2013; Schleider et al., 2014) and the possibility
a trigger(s), and significant functional impair- of anxiety’s stability or even worsening trajectory
ment associated with these emotions and result- over time (Cummings et al., 2014). For example,
ing behaviors (American Psychological it appears likely that child anxiety is associated
Association, 2013). Youth presenting with anxi- with onset of depression symptoms (Schleider
ety symptoms may meet full or partial criteria for et al., 2014). Three pathways have been identified
a number of DSM-V diagnoses simultaneously to explain the temporal relationships between
(Beesdo et al., 2009), and differentiation between anxiety and depressive disorder symptomatology.
such often requires detailed and time-consuming Across development, anxiety may lead to depres-
clinical interviews that may be further hampered sion, anxiety and depression may co-occur, or
by difficulty obtaining youth self-reports, ambig- depression results in anxiety (Cummings et al.,
uous diagnostic thresholds, or discrepant reports 2014). For example, youth with anxiety concerns
across informants (Beesdo et al., 2009). may be overwhelmed by their ruminative
Pediatric mental health disorders are highly thoughts and may withdraw or avoid triggering
prevalent and co-occur at high rates in children situations, leading to decreased peer interaction,
and adolescents (Kendall et al., 2010; decreased self-esteem, and depressive symptoms
Mohammadi et al., 2020). A meta-analysis con- (Garber & Weersing, 2010). As compared to
ducted between 1985 and 2012 examining youth single-disorder diagnoses (e.g., anxiety or depres-
mental health disorders across 27 countries found sion alone), comorbid anxiety and depression are
the worldwide prevalence rate of clinically sig- associated with more functional impairment,
nificant anxiety disorders in youth was 6.5% more frequent suicide attempts, increased service
(Polanczyk et al., 2015). Separation anxiety dis- utilization, sleep disturbances, and additional
order is commonly implicated as one of the earli- comorbidities such as substance use disorders
est appearing anxiety disorders in youth and is and conduct problems (Gallerani et al., 2010;
estimated to have a prevalence of 5.3% in youth Sarchiapone, 2013; Schleider et al., 2014).
ages 6–18, though prevalence rates are higher in Anxiety disorders in youth may also present
children ages 6–9 (Mohammadi et al., 2020). with a wealth of other comorbidities, such as
Mohammadi et al. (2020) found that 16% and obsessive-compulsive disorders (OCD), attention
19.3% of youth who met criteria for separation deficit hyperactivity disorder (ADHD), opposi-
anxiety disorder later met criteria for generalized tional defiant disorder (ODD), or eating disorder.
anxiety disorder and social anxiety disorder, Research suggests that generalized anxiety disor-
respectively, although previous studies have der (GAD) and OCD are “near-neighbor” disor-
found even higher rates (Spence et al., 2018). ders with similar presentations (e.g., repetitive
Such data has supported the hypothesis that the and distressing cognitions related to an a nticipated
9 Transdiagnostic Treatment Models for Child and Adolescent Anxiety Disorders 127
event), shared mechanisms (e.g., intolerance of anxiety disorders (Chu & Harrison, 2007), such
uncertainty), and common etiological pathways that treatments can be better personalized and
(Comer et al., 2004). Youth with ADHD and a adapted to target mechanisms that are particu-
comorbid internalizing or externalizing disorder larly dominant in each individual youths’ presen-
experience greater difficulties with social func- tation via specific intervention elements
tioning or academic performance, compared to (Nolen-Hoeksema & Watkins, 2011).
youth with ADHD alone (Booster et al., 2012), Transdiagnostic features or mechanisms may
and youth with behavioral problems such as be described as the “tendency to adopt particular
ODD or conduct disorder have an increased risk styles of responding to situations, such as a pes-
of experiencing anxiety or depression (Ollendick simistic attributional style, emotion regulation
et al., 2008). Many similar personality character- tendencies like chronic suppression, or personal-
istics have been implicated in anxiety and ity characteristics such as neuroticism or negative
anorexia nervosa, such as rigidity, perfectionism, affectivity” (Nolen-Hoeksema & Watkins, 2011,
and avoidance of perceived harm, potentially p. 594). One possible mechanism in anxiety is
explaining comorbidities and the causal mecha- neuroticism, a broad, higher-order trait that pre-
nisms between these two disorders (Hildebrandt disposes an individual to experience increased
et al., 2012). overall negative affect. According to Barlow
Evidence from a range of fields suggests that et al. (2014), individuals with higher levels of
the development and maintenance of pediatric neuroticism experience greater levels of distress
mental health disorders are due to the presence in response to internal and external cues and
and interaction of genetic and neurobiological therefore tend to perceive the world as an unsafe
factors (Weems et al., 2005), cognitive and place, leading them to feel incapable of coping
behavioral factors (e.g., neuroticism/negative with their stress (Barlow et al., 2014; Simons &
affect (Beesdo et al., 2009)), and environmental Gaher, 2005; Tull & Gratz, 2008). Over time,
factors such as stressful life events and parenting these individuals develop lower self-efficacy to
behaviors (Beesdo et al., 2009). Because of the manage their strong emotions and have difficulty
similar etiologies and shared constructs of anxi- foreseeing positive outcomes (Sauer-Zavala
ety and other related disorders, transdiagnostic et al., 2020). Individuals with higher neuroticism
treatments for youth anxiety that possess the abil- then learn to utilize behavioral strategies to pre-
ity to pivot or adapt to near-neighbor disorders vent or deescalate the experience of strong dis-
and presentations (e.g., depression or irritability) tressing emotions, such as avoidance and
may be a simple and efficient solution to these cognitive suppression (Sherman & Ehrenreich-
challenges. May, 2020).
Neuroticism has been implicated in the devel-
opment of a range of psychopathologies in youth
Evidence for Transdiagnostic (Norton & Paulus, 2017) and is associated with
Mechanisms other transdiagnostic mechanisms, such as dis-
tress tolerance (Tonarely et al., 2020b), psycho-
The efficacy of transdiagnostic treatments in logical inflexibility, and emotion dysregulation
ameliorating diverse symptom clusters is posited (Norton & Paulus, 2017). Although neuroticism
to be the result of successfully targeting higher- and other related mechanisms can be method-
order factors in treatment (Chu, 2012) and thus ologically difficult to study in youth due to the
improving cognitive and behavioral patterns that internal nature of the construct and differences in
maintain related clusters of psychopathology. An observable facets of neuroticism in developing
increasing body of research has focused on iden- youth compared to adults (e.g., irritability versus
tifying and understanding underlying mecha- sadness or anxiety in young children (Brandes
nisms associated with the development and et al., 2019)), aspects of neuroticism have been
maintenance of emotional disorders, including reliably measured in children as young as 3 years
old (Tackett, 2006) and in large samples of decrease the intensity of their experience
diverse youth (Brandes et al., 2019). These find- (Silverman et al., 1991) negatively reinforcing
ings suggest that general, trait negative affectivity efforts to suppress or avoid the experience. AS has
may account for the majority of the overlaps been reliably measured using the Child Anxiety
among common emotional problems and that Sensitivity Index (CASI) (Silverman et al., 1991)
neuroticism and its facets are immanent through- in both clinical and nonclinical children and ado-
out the various spectra of psychopathology (e.g., lescents ages 7–17 years old (Chorpita &
internalizing, thought disorder, disinhibited or Daleiden, 2000). Behavioral studies of AS in
antagonistic externalizing, etc. (Brandes et al., youth show that the CASI can also predict state
2019; Kotov et al., 2017)). anxiety and changes in fear responses to a chal-
Distress tolerance, or the ability to tolerate lenge task (MacIntyre, 2001; Rabian et al., 1999).
uncomfortable states (Zvolensky et al., 2010), has In youth, AS prospectively predicts anxiety disor-
received a great deal of attention in the transdiag- ders (Schmidt et al., 2010). There is some evi-
nostic literature (Wolitzky-Taylor et al., 2015). dence that DT and AS together form a higher
Tonarely and Ehrenreich-May (2019) recently order construct of affect intolerance (Bernstein
validated a self-report measure of distress toler- et al., 2009; Keough et al., 2010); however, more
ance (DT) in samples of clinical and nonclinical research is needed to clarify the validity of these
youth (Tonarely & Ehrenreich-May, 2019). hierarchical relationships in children and adoles-
Behavioral measures of DT in youth may effec- cents and their relationships to specific anxiety
tively measure DT (Tonarely et al., 2020a); how- symptomatology (Shaw et al., 2021).
ever, findings suggest that youth’s perception of Other features of emotion regulation have also
their ability to handle distressing emotions may been studied as transdiagnostic features.
differ from their actual persistence on behavioral Understanding and/or labeling of affective states
tasks that incite frustration (Tonarely et al., 2020a). (Kranzler et al., 2016), dysregulated expression of
Similar to distress tolerance, intolerance of uncer- sadness and anger, and ruminative responses to
tainty (IUC) has also been shown to be transdiag- distress have been implicated as transdiagnostic
nostic in youth with anxiety disorders. IUC has factors that predict anxiety and other emotional
been measured with the adapted Intolerance of disorder symptoms (e.g., aggressive behavior, eat-
Uncertainty Index-A for Children (Rifkin & ing pathology (McLaughlin et al., 2011)).
Kendall, 2020) and the Intolerance of Uncertainty Rumination, which can be thought of as an anxi-
Scale for Children (IUSC (Comer et al., 2009)). ety-related behavior and/or as cognitive avoidance
IUSC scores have been shown to predict overall (Jacobson et al., 2001), has also been identified as
anxiety severity, regardless of diagnostic category an important transdiagnostic feature in anxiety and
(Read et al., 2013). Evidence shows that IUC is a other internalizing disorders (Klemanski et al.,
transdiagnostic feature that is associated with anx- 2017). Studies of rumination show that this cogni-
iety severity, rather than GAD specifically (Cowie tive action may partially explain the co-occurrence
et al., 2018; Hearn et al., 2017; McEvoy et al., of internalizing symptoms and other emotionally
2019; Rifkin & Kendall, 2020). driven behaviors (e.g., aggressive behavior) and
Anxiety sensitivity (AS), the fear of anxiety- that rumination is related to executive function
related sensations, has been empirically supported patterns seen in internalizing disorders, supporting
as a transdiagnostic feature seen across youth the transdiagnostic nature of this thinking pattern
anxiety disorders (Noël & Francis, 2011; Wauthia (Chu et al., 2016; McLaughlin et al., 2014; Snyder
et al., 2019). Fear of physiological anxiety-related et al., 2019; Verstraeten et al., 2011).
sensations, such as physical feelings (e.g., racing There are also transdiagnostic features that
heart) and observable symptoms (e.g., blushing), can be categorized as cognitive deficits or biases
in the absence of a danger or threat, leads one to in information processing (e.g., attentional
search for a source of their experience, reinforc- biases, working memory deficits) that have been
ing a cognitive bias, and to take some action to identified and validated in children and adoles-
cents with anxiety, other internalizing disorders, individual anxiety disorders. For example, a child
and externalizing disorders (Schweizer et al., with comorbid panic disorder and specific phobia
2020). Cognitive vulnerabilities can include dys- of vomiting may perceive somatic/physical feel-
functional attitudes (Abela & Sullivan, 2003), ings or body sensations more generally as threat-
negative inferential style (Hankin & Abramson, ening, further explaining elevated comorbidity
2002; Lakdawalla et al., 2007), and self-criticism rates between the two diagnoses (Leyfer et al.,
(Abela & Taylor, 2003). Attentional bias toward 2013). Without treatment that targets heightened
threatening information, threat appraisal, mem- anxiety sensitivity and avoidance, this cycle of
ory, and learning biases all appear to confer risk avoidance and maladaptive behaviors might con-
for child anxiety disorders (Muris & Field, 2008; tinue into adolescence and adulthood. When
Rheingold et al., 2003; Schmidtendorf et al., avoidance behaviors continue across develop-
2018). Interpretation bias can be reliably assessed ment, negative emotion and fears can continue to
using an ambiguous vignette paradigm (Fliek intensify, worsen, and/or generalize to other
et al., 2019), which utilizes a series of descrip- related domains or situations.
tions of everyday situations and asks children to Forms of avoidance, or behaviors that result in
score the perceived level or threat or indicate how an individual not engaging in or retreating from a
they would respond if they encountered them fear-evoking or distressing situation (Chu et al.,
(Bell-Dolan, 1995; Bögels & Zigterman, 2000; 2016), are characterized by their negative rein-
Cannon & Weems, 2010; Muris et al., 2009; forcement function and are a main target of most
Waters & Craske, 2016). Confirmation bias, or evidence-based cognitive-behavioral interven-
the tendency to selectively search for information tions for anxiety. Avoidant behaviors can be
that coincides with one’s views while ignoring thought of as maladaptive emotion regulation
disconfirming information (Muris et al., 2014), attempts, as they are often engaged in out of
can also be reliably measured via a task assess- attempts to decrease the intensity or avoid the
ment. Children are asked to select additional, experience of strong emotions. The use of avoid-
positive, or negative information about a novel, ant behaviors, including types of experiential or
which potentially includes threatening stimulus situational avoidance, not only alleviates anxiety,
or situation (Dibbets et al., 2015; Muris et al., but it also further reduces opportunities for posi-
2009; Remmerswaal et al., 2014). The tendency tive reinforcement and safety or inhibitory learn-
to pay more attention to threatening or dangerous ing (Ferster, 1973; Jacobson et al., 2001; McGuire
stimuli (i.e., attention bias), perceive situations as & Storch, 2019). Avoidant behaviors can be mea-
being more threatening or dangerous than they sured by self-report and parent report measures
actually are (i.e., interpretation bias), and selec- and are related to other forms of avoidance in
tively recall memories similar to the causes of youth with various anxiety disorders (Whiteside
anxiety (i.e., memory bias) further biases the et al., 2013).
interpretation of ambiguous situations and has all Avoidance can occur either behaviorally (e.g.,
been supported as transdiagnostic processes in fleeing, procrastination) or cognitively (e.g., wor-
youth with different anxiety disorders and comor- rying, distracting) and can also include the use of
bid depressive disorders (Hankin et al., 2010; safety behaviors (e.g., hunching or shrinking pos-
Salum et al., 2013; Waters & Craske, 2016). tures), objects (e.g., carrying water or benzodiaz-
epine in case of a panic attack), or people (e.g.,
only attending a birthday party with a close friend).
Transdiagnostic Conceptualization These behaviors may also include aggression and
of Child Anxiety irritability or behaviors that other caregivers do to
accommodate child anxiety. From a behavioral
A transdiagnostic conceptualization of pediatric perspective, regardless of the specific diagnostic
anxiety disorders accounts for the behavioral ten- domain, behaviors that decrease the intensity of
dencies or cognitions commonly seen across strong emotions (e.g., safety behaviors, reassur-
ance seeking, overt avoidance) temporarily assessment (Beesdo et al., 2009). Transdiagnostic
decrease distress, fear, or anxiety caused by a pre- interventions may be inclusive of differing theo-
senting stimulus or perceived threat, thereby nega- retical approaches to treatment, including accep-
tively reinforcing maladaptive behavioral patterns tance and commitment therapy (ACT), dialectical
(Krypotos et al., 2015). For example, escaping behavioral therapy (DBT), and cognitive-
from a classroom or avoiding school may cause behavioral therapies (CBT). Transdiagnostic
momentary relief, but the child becomes condi- approaches often possess unique advantages in
tioned to avoid feared or unpleasant stimuli treating a range of emotional disorders beyond
(Blakey & Abramowitz, 2016), whether it be a anxiety alone (Dalgleish et al., 2020), may have
performance, an exam in school, or the sensation increased feasibility, and could alleviate burdens
of his/her heart racing. This can also reinforce a in training, dissemination, and implementation
child’s low self-efficacy or belief in his/her ability (Ehrenreich-May & Chu, 2013). It is known that
to cope with a feared situation or trigger. Familial evidence-based treatment (EBT) fidelity impacts
accommodation in the context of pediatric anxiety treatment outcomes, but the flexibility of some
disorders occurs when caregivers or other family transdiagnostic interventions also allows for
members modify their own behaviors to conform increased adherence to an intervention under
to and reduce their youth’s distress surrounding a challenging treatment conditions, while also
feared stimulus (Thompson-Hollands et al., 2014). maintaining a manualized approach (Ehrenreich-
Family accommodation has also been identified as May & Chu, 2013; McHugh et al., 2009).
a maintaining factor of youth anxiety that may Both the Coping Cat (Kendall, 2006) and the
even intensify or worsen symptoms across time Modular Approach to Therapy for Children with
(La Buissonnière-Ariza et al., 2018). Anxious Anxiety, Depression, Trauma, or Conduct
youth may also attempt to cope with the intensity Problems (MATCH-ADTC) (Chorpita & Weisz,
of their emotions through excessive reassurance 2009) may be conceptualized as both evidence-
seeking, which also reinforces a child’s anxious based and multidiagnostic treatments that can be
symptoms (Varela et al., 2009). applied to individual anxiety presentations and,
These symptoms, related behaviors, and their particularly for MATCH-ADTC, may serve as an
associated distress cause clinically significant efficient and targeted option to treat closely
functional impairment in a range of settings, related disorders (Chorpita et al., 2017; Podell
including in the home, school, and other social set- et al., 2010). The Coping Cat (Kendall, 2006)
tings (Beesdo et al., 2009). Transdiagnostic inter- was designed to simultaneously target a range of
ventions seek to identify these cycles of avoidance youth anxiety disorders (GAD, social phobia,
and target the mechanisms that are contributing separation anxiety disorder), and options for flex-
the intensity and intolerability of these emotional ible delivery and adaptations of the intervention
states. To note, in all clinical conceptualizations are available (Beidas et al., 2010). In a random-
and treatment approaches, it is also important to ized controlled trial, Weisz and colleagues found
distinguish normative versus clinically impairing that MATCH-ADTC showed better outcomes
avoidance and distress in children. than treatment as usual or another evidence-
based treatment in a sample of treating treatment-
seeking youth in a community (Weisz et al.,
Transdiagnostic Interventions 2012) and used an algorithm-based treatment
model to allow clinicians to easily pivot between
Support for transdiagnostic approaches to anxi- anxiety symptoms and other problem areas, as
ety may be gleaned from research with adults, needed.
evidence for shared mechanisms of youth anxiety The primary transdiagnostic approach to anx-
and related emotional disorders, and the chal- iety and related disorders is the Unified Protocol
lenges in diagnosing mental health disorders in for Transdiagnostic Treatment of Emotional
settings without detailed or formal diagnostic Disorders in Children and Adolescents (UP-C/A)
(Ehrenreich-May et al., 2017). Developed simul- (Kennedy et al., 2018). When compared to an
taneously with the adult Unified Protocol (UP) anxiety-focused intervention, the UP-C was as
(Barlow et al., 2017), the UP-C/A are transdiag- efficacious in reducing anxiety symptoms as the
nostic manuals for children and adolescents, anxiety-focused treatment and indicated longer-
respectively, with emotional disorders. The term remission in symptoms (Kennedy et al.,
UP-C/A broadly employ cognitive-behavioral 2018). Further investigations have shown the effi-
therapy (CBT) techniques, with an emphasis on cacy of the UP-C/A in reducing obsessive-
behavioral principles of change. CBT and mind- compulsive symptoms, depression, and serious
fulness strategies are integrated into a modular mental illnesses (e.g., bipolar disorder, psycho-
approach to treatment in the UP-C/A that includes sis, schizophrenia), though additional research on
both parent-directed and child-focused materials, long-term outcomes is warranted on the ways in
which can be adapted to fit the needs of an indi- which applications and adaptations of the UP-C
vidual client or to be delivered in a group setting. and UP-A may be most efficacious. In an open
The UP-C/A utilize the Top Problems, an idio- trial of youth who were treated with the UP-C
graphic weekly progress monitoring (Weisz and UP-A (n = 170), obsessive-compulsive
et al., 2011) to track changes in nondisorder- symptoms significantly decreased throughout the
specific “emotional behaviors” (e.g., avoidance, course of treatment, by both parent and child
reassurance seeking, angry behaviors). Skills are self-reports (Shaw et al., 2020). Preliminary data
introduced and then adapted such that they can has also shown that the UP-A is effective in tar-
target a range of emotional behaviors related to geting adolescents at high risk for serious mental
the clinical presentation. For example, to increase illnesses, such as psychosis risk or unspecified
emotion regulation and improve distress toler- bipolar disorder (Weintraub et al., 2020).
ance, the UP-C/A employ emotional awareness Applications for the UP are also being explored
and interoceptive exposures, as well as “opposite to treat borderline personality disorder, eating
action” skills used to foster a personalized behav- disorders, nonsuicidal self-injurious behaviors,
ioral activation or exposure plan that can be and severe pediatric irritability (Bentley, 2017;
adapted to fit the needs of the child. Further, Hawks et al., 2020; Lopez et al., 2015). See
mindfulness skills such as present moment Table 9.1 for an overview of the extent efficacy
awareness and nonjudgmental awareness are literature on the UP-C/A.
aimed at decreasing mechanisms such as rumina- Other EBTs, such as ACT and DBT, also aim
tion and repetitive negative thinking, constructs to target transdiagnostic features and have been
commonly seen in youth with a range of anxiety shown to address a range of symptom clusters in
and related disorders. youth (Swain et al., 2015). When compared to
Overall, investigations into the efficacy of the CBT and a waitlist-controlled condition in youth
UP-C/A in a range of settings have shown signifi- with primary or comorbid anxiety disorder diag-
cant success in treating youth with a broad range noses, ACT showed similar outcomes to CBT in
of mental health concerns. In an open trial utiliz- significantly reducing youth anxiety by child and
ing the UP-C in a group setting, by both child and parent reports (Hancock et al., 2018). Research
caregiver reports, children experienced a signifi- also suggests that DBT for adolescents (DBT-A)
cant reduction in anxiety symptoms across disor- can be utilized to treat both internalizing and
ders diagnosed at baseline (e.g., GAD and social externalizing symptomologies in youth
anxiety, GAD and separation anxiety disorder (Fleischhaker et al., 2011; Nelson-Gray et al.,
(Ehrenreich-May & Bilek, 2012)). Further 2006), in addition to the borderline features for
research on the efficacy of the UP-C in targeting which it was originally developed. In adults,
anxiety disorders indicates reduction in child- some results have also shown that DBT skills
rated anxiety from pretreatment to post-treatment; (e.g., mindfulness, psychological flexibility)
however, social anxiety symptoms specifically have led to reduction in anxiety symptoms more
predicted poorer response to the intervention specifically (Webb et al., 2016).
Table 9.1 Notable studies supporting the efficacy of the UP, UP-A, and UP-C
Citation Design Treatment Outcome
Barlow et al. (2017) and RCT UP vs. Participants who received the UP showed equal
Eustis et al. (2020) single- improvements in symptomology to those who
disorder received a single-disorder treatment at post-
treatment treatment and at a 12-month follow-up.
Participants in the UP condition were also more
likely to complete treatment.
Bilek and Ehrenreich-May Open trial UP-C Children and caregivers reported significant
(2012) reductions in anxiety and depressive symptoms
from pre- to post-treatment.
Kennedy, Ehrenreich-May, RCT UP-C vs. All youth showed significant declines in anxiety
and Bilek (2018) anxiety- symptoms and the groups did not significantly
focused differ in their improvements at post-treatment. At
CBT follow-up, those in the UP-C condition showed
greater long-term symptom remission than those
who received anxiety-focused CBT.
Ehrenreich-May et al. (2017) Waitlist- UP-A vs. Adolescents treated with the UP-A showed
and Queen, Barlow, and controlled RCT waitlist greater improvements in anxiety, depressive, and
Ehrenreich-May (2014) global severity at post-treatment and 6-month
follow-up than adolescents in the waitlist
condition.
Ehrenreich, Goldstein, Multiple UP-A Adolescents with clinical emotional disorders
Wright, and Barlow (2009), baseline and showed significant improvement in symptoms
Sherman and Ehrenreich- open trial from pre- to post-treatment.
May (2020) and Trosper,
Buzzella, Bennett, and
Ehrenreich (2009)
Shaw et al. (2020) Open trial UP-C and Obsessive-compulsive symptoms (OCS)
UP-A significantly decreased from pre- to
post-treatment.
García-Escalera et al. (2020) Randomized UP-A Youth who received an adaptation of the UP-A for
waitlist- school-based preventative intervention showed
controlled trial effective reported reductions in anxiety and
depression symptoms at post-treatment and a later
follow-up.
Kennedy et al. (2021) UPC-SC A piloted stepped-care version of the UP-C
(UPC-SC) showed improvements in a range of
emotional disorder symptoms in youth.
Researchers globally are disseminating trans- low burden, and efficient method to treating large
diagnostic interventions in brief formats that samples of youth populations displaying a range
could be widely implemented to large samples of of co-occurring disorders and symptom variabili-
youth in a range of settings (Martin et al., 2018). ties, including anxiety and depression
For example, an ongoing school-based random- (Ehrenreich-May & Chu, 2013; Schleider &
ized controlled trial (RCT) in New Delhi, India, Weisz, 2018). These nonintensive interventions
was designed to target adolescents who are show promise in robustly improving youth anxi-
reporting any elevated or persistent mental health ety and depression immediately following the
difficulties and their associated distress or impair- session and 9 months later (Schleider & Weisz,
ing effects using the basics of the MATCH- 2018). The UP-A has also been adapted for pre-
ADTC framework as a starting point for ventative intervention and implemented in school
adaptation (Michelson et al., 2020; Parikh et al., settings, with youth reporting significant declines
2019). Single-session interventions (SSIs) are in both depression and anxiety from pre- to post-
also increasing in use as they offer an accessible, treatment (García-Escalera et al., 2020).
FRIENDS, a universal, school-based preventa- American Psychiatric Association. (1980). Diagnostic

and statistical manual of mental disorders (3rd ed.,
tive intervention for Australian youth displaying text rev.).
elevated anxiety and depressive symptoms, has American Psychiatric Association. (2013). Diagnostic
also shown effective outcomes for adolescents at and statistical manual of mental disorders (5th ed.).
long-term follow-ups (Barrett et al., 2006). Barlow, D. H., Allen, L. B., & Choate, M. L. (2004).
Toward a unified treatment for emotional disorders.
Preliminary outcomes for stepped care models of Behavior Therapy, 35(2), 205–230.
cognitive-behavioral interventions have shown Barlow, D. H., Ellard, K. K., Sauer-Zavala, S., Bullis,
positive outcomes for anxiety and depressive J. R., & Carl, J. R. (2014). The origins of neuroticism.
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Barlow, D. H., Farchione, T. J., Sauer-Zavala, S., Latin,
et al., 2017; Salloum et al., 2016). H. M., Ellard, K. K., Bullis, J. R., et al. (2017). Unified
protocol for transdiagnostic treatment of emotional
disorders: Therapist guide. Oxford University Press.
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M. (2006). Long-term outcomes of an Australian
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In the development of pediatric anxiety disorders symptoms in children and youth: An evaluation of
and across diagnostic categories, “common ele- the friends program. Journal of Clinical Child and
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Beesdo, K., Knappe, S., & Pine, D. S. (2009). Anxiety
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ity, distress intolerance, cognitive inflexibility, Developmental issues and implications for DSM-V.
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J. M., & Kendall, P. C. (2010). Flexible applications of
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24(1), 2–10.
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based treatment approach, impairing anxiety Transdiagnostic treatment to nonsuicidal self-injury
concerns and conditions that often co-occur with and co-occurring emotional disorders: A case illustra-
anxiety may be treated more effectively than uti- tion. Journal of Clinical Psychology, 73(5), 547–558.
Bernstein, A., Zvolensky, M. J., Vujanovic, A. A., &
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presenting with anxiety disorders may also be tress tolerance, and discomfort intolerance: A hier-
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Bilek, E. L., & Ehrenreich-May, J. (2012). An open trial
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Part II
Differential Diagnosis of Attention
Deficit Hyperactivity Disorder 10
(ADHD) in Child and Adolescent
Anxiety
Alasdair Vance, Jo Winther, and Elham Shoorcheh
Anxiety disorders and attention deficit hyperac- main presentations of ADHD, ADHD-combined
tivity disorder (ADHD) are both common condi- presentation (ADHD-CT), ADHD-hyperactive-
tions in children and adolescents. Furthermore, impulsive presentation (ADHD-HI) and ADHD-
there is a known greater-than-chance association inattentive presentation (ADHD-IA) (American
between them, which is evident in epidemiologi- Psychiatric Association, 2013). A patient must
cal and clinical studies (Anderson et al., 1987; present with more than six symptoms of inatten-
Jensen et al., 2001; Pliszka, 2019). This chapter tion and less than six symptoms of hyperactivity-
explores how ADHD affects the diagnosis, clini- impulsiveness to meet the threshold criteria for
cal presentation, assessment and treatment of ADHD-IA, more than six symptoms of
anxiety disorders and emerging mechanisms to hyperactivity- impulsiveness and less than six
deepen our understanding of these effects. There symptoms of inattention to meet the threshold
is a particular emphasis on key differential diag- criteria for ADHD-HI and more than six symp-
noses to consider in a comprehensive approach to toms of inattention and hyperactivity-
assessment and composing more specific and tar- impulsiveness to meet the threshold criteria for
geted treatment plans for young people with anx- ADHD-CT. If the patient is 17 years and older,
iety disorders and comorbid ADHD. then the threshold is reduced to 5 symptoms.
Further criteria stipulate that the symptoms must
have been present and caused some clinically sig-
DHD and the Diagnosis of Anxiety
A nificant impairment before the child was 12 years
Disorders of age, and the impairment must be present in 2
or more settings over the preceding 6 months.
ADHD is categorised in the neurodevelopmental The diagnosis of ADHD is made only if the
disorder group and characterised by developmen- symptoms are not better accounted for by any
tally inappropriate levels of inattention and/or other disorders such as a psychotic disorder,
impulsiveness-overactivity (American mood disorder, personality change disorder due
Psychiatric Association, 2013). There are three to a medical condition and/or any substance-
related disorder.
A. Vance (*) · J. Winther · E. Shoorcheh Similarly, a number of different anxiety disor-
Academic Child Psychiatry Unit, Department of ders are recognised in the current Diagnostic and
Paediatrics, University of Melbourne, Royal
Statistical Manual for Mental Disorders (DSM)
Children’s Hospital,
Parkville, Melbourne, VIC, Australia nosology (American Psychiatric Association,
e-mail: avance@unimelb.edu.au 2013). Importantly, like the three ADHD
https://doi.org/10.1007/978-3-031-14080-8_10
142 A. Vance et al.
s ubtypes, they share a number of clinical, aetio- ADHD followed by ADHD-CT, while ADHD-CT
logical risk factors and treatment response fea- predominates in clinical samples (Biederman
tures in common. However, there are also key et al., 1991a; Taylor et al., 1986). This is broadly
differences: for example, generalised anxiety dis- consistent with increased rates of ODD associ-
order (GAD), separation anxiety disorder (SAD), ated with ADHD-CT compared to ADHD-IA
social anxiety disorder (SoAD) and specific pho- (Cantwell & Baker, 1992), for ODD is a common
bia (SpPh) form a coherent group of anxiety dis- reason for a child’s or adolescent’s referral to
orders that are closely aligned (Fonesca & Perrin, mental health services (Loeber et al., 2000). Of
2001; Vance, 2005). In contrast, obsessive com- course, there are other factors that also affect this
pulsive disorder (OCD), a former anxiety disor- difference; these are beyond the scope of this
der now categorised with ADHD in the chapter. Approximately, 30–40% of patients with
neurodevelopmental disorder group, has a dis- ADHD will have comorbid anxiety disorder(s)
tinctive clinical presentation, set of aetiological (Biederman et al., 1996), while 15–30% of those
risk factors and psychological and/or medication with anxiety disorders are noted to have ADHD
treatment responses (Fonesca & Perrin, 2001). (Last et al., 1991). Twenty-five to thirty-three
This essential heterogeneity in both ADHD and percent is a consistent average range from clini-
anxiety disorders presents a significant hurdle for cal and epidemiological samples (Pliszka, 2019),
the clinician and the researcher to overcome, for confirming the greater-than-chance association
instance, the sheer number of possible ADHD of anxiety disorders with ADHD. Interestingly,
subtype and anxiety disorder combinations to be child, adolescent and recently adult samples con-
considered and the potential additive risk or ame- firm the enduring association between anxiety
liorating effect of given different combinations of disorders and ADHD across key developmental
ADHD and anxiety disorders (Fonesca & Perrin, stages (Schatz & Rostain, 2006). Also, this asso-
2001; Vance, 2005). For example, children with ciation is evident across different social groups,
ADHD and anxiety may be less likely to develop cultures and nations (Buyn et al., 2006). Further,
comorbid oppositional defiant disorder (ODD) or gender does not moderate the association between
conduct disorder (CD) symptoms (Bilgic et al., anxiety disorders and ADHD in children, adoles-
2013) while those with panic disorder (PD) may cents or adults (Biederman et al., 1991b).
be more likely to develop comorbid major depres- Early studies noted the robust association
sive disorder (MDD) with or without persistent between anxiety disorders and ADHD-IA com-
depressive disorder (PDD) (Bittner et al., 2004). pared to ADHD-CT (Lahey et al., 1988; Stanford
Nevertheless, while much research is yet to be & Hynd, 1994). In contrast, studies using clinical
done to elucidate these complexities, there have samples have failed to demonstrate any differ-
been significant gains in theoretical understand- ences between these two ADHD subtypes
ing, clinical knowledge and treatment approaches (Willcutt et al., 1999; Wolraich et al., 1996).
over the past decade (D’Agati et al., 2019). Indeed, it appears that ADHD-IA and ADHD-CT,
Epidemiological studies suggest point preva- the two most common subtypes of ADHD in epi-
lence rates from 2% to 24% for anxiety disorders, demiological and clinical samples, do not differ
defined in various ways, categorically and/or in their greater-than-chance association with anx-
dimensionally, and from 1% to 17% for ADHD, iety disorders or in the specific types of anxiety
again variably defined, categorically and/or disorders with which they are comorbid.
dimensionally (Tannock, 2009). Categorical Interestingly, parent- and child-reported anxiety
diagnostic rates are almost always lower than disorders have similarities and differences from
those that are questionnaire-derived. GAD, SpPh, childhood into adolescence, although their under-
SAD and SoAD are the four most common anxi- lying nature is congruent (Vance, 2005).
ety disorders, while PD is less common, particu- Cantwell et al. (1992) noted that increased
larly prepuberty. In epidemiological samples, rates of SAD were reported with ADHD-CT
ADHD-IA is the most common subtype of (DSM-III equivalent) compared to
10 Differential Diagnosis of Attention Deficit Hyperactivity Disorder (ADHD) in Child and Adolescent… 143
ADHD-IA. Our group has reported point preva- ders (Biederman et al., 2006; Bowen et al., 2008;
lence rates of 20–40% child-self-reported anxiety Melegari et al., 2018). These conditions invari-
disorders in medication naïve children with ably confer additional functional impairment in
ADHD-CT (Vance et al., 1999). We have also one or more academic, social, home or occupa-
noted the weak correlation between parent- and tional domains. In particular, impaired social
child-reported anxiety disorders and the decrease functioning manifest via worse social skills and
in child-reported anxiety disorders over time, increased social problems has been outlined in
while there is no change in parent-reported anxi- young people with ADHD and anxiety (Bowen
ety disorders (Vance et al., 2002). Furthermore, et al., 2008; Bishop et al., 2019). However, devel-
we have reported that the child self-report of opmental stage, ADHD subtype, gender and
SAD was the only parent- or child-self-reported additional comorbidities are crucial determinants
anxiety disorder to be significantly increased in affecting social functioning (Bishop et al., 2019).
the anxiety disorders and ADHD-CT compared Hechtman et al. (2016) reported that young adults
to the anxiety disorders alone group (Vance, followed up from the Multimodal Treatment
2005). This suggests an additive or multiplicative Study of Children with ADHD (MTA) study with
effect between SAD and ADHD-CT that requires emotional outcomes that included ADHD and
further investigation using epidemiological data anxiety, where ADHD symptoms were desistent,
with larger numbers, particularly in the anxiety had a functional outcome no different from the
disorders alone group. These divergent parent- local normative comparison group.
and child-reported findings are consistent with Developmental stage is also crucial for under-
studies that have shown that only approximately standing the potential risk or protective effects
50% of children with self-reported anxiety have that ADHD and anxiety may exert: worse work-
been noted to also be reported with anxiety by ing memory (WM) deficits during adolescence
their parents (Pliszka, 1992) and that the parent and worse sleep difficulties in adulthood but bet-
and child report may have different origins: the ter inhibitory function in childhood (D’Agati
parent report of their given child’s anxiety et al., 2019). Similarly, Bilgic et al. (2013) have
disorder(s) may represent their child’s ‘negative reported that anxiety sensitivity may decrease
affectivity and associated behavioural problems’ conduct disorder symptoms in childhood and
rather than ‘neurotic anxiety suffered by children adolescence, and Winther et al. (2020) have out-
with anxiety disorders alone’ (March et al., lined that ADHD and GAD in childhood are pro-
2000). This is consistent with Pliszka’s (2019) spectively linked with lower rates of ODD in
assertion that the presence of comorbid ODD/CD adolescence. Recently, Shoorcheh et al. (2018)
may explain this difference in parent and child reported that spatial WM, especially its strategy
reports of anxiety in ADHD. Moreover, signifi- component involved in planning, organising and
cant clinical correlates, such as levels of self- prioritising information held in WM, were better
confidence and impairments in activities of daily in young people with ADHD (all three presenta-
living, may be associated with the child anxiety tions) and anxiety compared to ADHD alone at
self-report alone (Tannock, 1994). follow-up. They completed a 3-year longitudinal
Anxiety disorders and ADHD can persist or study of prepubertal children with ADHD (all
actually worsen from childhood into adolescence presentations), successfully treated with stimu-
(Barkley et al., 1996) and are associated with lant medication using a standardised regimen,
greater symptom severity and worse levels of then followed up 3 years later postpuberty. The
impairment (Bowen et al., 2008). Furthermore, ADHD with/without anxiety groups did not dif-
additional comorbid conditions may preexist, for fer with respect to their medication status (medi-
example, autistic spectrum disorder (ASD) cation used, dose received, duration medication
(Gordon-Lipkin et al., 2018), or develop, such as treatment, responder status). The two groups did
sleep problems (Beriault et al., 2018; D’Agati not differ on any confounding factors (e.g. age,
et al., 2019), ODD/CD and/or depressive disor- gender, full-scale IQ, social adversity status) that
144 A. Vance et al.
may explain this cognitive difference. 2018). Vance et al. (2013) noted that there was no
Importantly, ADHD subtype may be linked with evidence of an additive effect of ADHD-CT and
differential cognitive benefits for spatial WM anxiety on impaired spatial WM, strategy and
(Ferrin & Vance, 2014): ADHD-CT and anxiety/ span performance in children and adolescents
depressive symptoms may be associated with a with ADHD-CT. However, anxiety disorders
better strategy performance, while ADHD-IA alone were associated with impaired spatial WM
and anxiety/depressive symptoms may be linked and cognitive spatial span performance compared
to better cognitive spatial span. Interestingly, to healthy control participants. In contrast, strat-
Gomez et al. (2014) outlined that worse verbal egy did not differ between children and adoles-
and spatial WM performance was associated with cents with anxiety disorders alone and healthy
increased depressive disorders (MDD and/or control participants, suggesting that with anxiety
PDD), implying that anxiety alone may be the cognitive span is the most affected component.
factor conferring a WM benefit. Further, these findings were age-independent.
The exact nature of comorbid anxiety disor- At the phenomenological level, option (4) is
ders with ADHD remains unclear. Current possi- supported by the greater-than-chance association
bilities include (1) the ADHD (usually ADHD-IA) of ODD with ADHD-CT, depressive disorders
symptoms being secondary to the primary anxi- and anxiety disorders as a replicated finding
ety disorder (e.g. DSM-IV GAD), (2) the anxiety (Angold et al., 1999). Maughan et al. (2004) have
disorders arising from a maladjustment of the also noted previous epidemiological studies that
patient to a primary ADHD (usually ADHD-CT), have reported this association and confirmed it
(3) both disorders arising from common biologi- using data from their own epidemiological study.
cal and/or psychosocial antecedent risk factors Within the ADHD-CT literature, the greater-
and (4) the association between both disorders than-chance association of ADHD-CT with
arising from their separate association with a ODD, depressive disorders and anxiety disorders
third disorder such as ODD, CD or depressive has also been noted (Lahey et al., 2000; Vance
disorders such as persistent depressive disorder et al., 2005). Vance et al. (2005) found that the
(PDD) and/or major depressive disorder (MDD). relationship between anxiety disorder symptoms
A number of lines of evidence are emerging to and ODD symptoms is mediated by the relation-
support options (3) and (4). The former is sup- ships between ADHD-CT symptoms, PDD
ported by accumulating evidence examining symptoms and ODD symptoms. This finding
underlying cognitive risk factors: ADHD and extends Angold et al.’s (1999) reported associa-
anxiety are associated with decreased processing tion of conduct disorder with anxiety disorders
speed, increased reaction times, increased via each disorder’s link with depressive disorders
response inhibition and worse WM performance by specifically demonstrating the association
in children and adolescents (Mayes et al., 2009; between ODD and PDD symptoms within a pri-
Bloemsma et al., 2013; Jarrett et al., 2016). mary school-age ADHD-CT sample.
Moreover, Van der Meer et al. (2018) reported A second line of evidence supporting option
that adolescents and young adults with ADHD (4) involves underlying biological risk factors.
and anxiety manifest decreased neural activity We examined the association of neurodevelop-
when performing a spatial WM task in brain mental deficits (NDD) with anxiety disorders,
regions subserving information gating (cerebel- ADHD-CT and PDD in primary school-age chil-
lum, striatum and thalamus). In contrast, other dren (Vance et al., 2006). The ADHD-CT and
studies investigating ADHD and anxiety in chil- PDD groups had significantly increased total
dren, adolescents and young adults have found no neurological subtle signs compared to the anxiety
WM differences, primarily due to methodologi- disorder group and the healthy control group.
cal differences in sample phenomenological defi- The anxiety disorder group also had significantly
nition and how WM is assessed (Adamo et al., increased neurological subtle signs compared to
2019; Villemonteix et al., 2017; Yurtbasi et al., the healthy control group. The findings replicated
earlier work by Taylor et al. (1991) and are con- & Albano, 1996) and by the parent and/or child
sistent with results reported by Piek et al. (1999). report of the total anxiety scores being greater
Shaffer et al.’s (1985) findings were extended than 1.5 standard deviations above the mean for
through demonstrating that (1) within the rubric a given child’s age and gender (Achenbach &
of ‘affective diagnoses’, PDD rather than anxiety Edelbrock, 1983; Reynolds & Richmond,
disorders may better explain the reported associ- 1985). A similar categorical and dimensional
ation between ‘emotional’ disturbance and neu- approach was used to define ADHD-CT and
rological ‘soft signs’ and (2) ‘emotional and separately PDD. The children were all stimu-
behavioural disturbances’ are associated with lant, anxiolytic and antidepressant medication
neurological subtle signs, as the strength of the naïve. All groups were matched for age, gender,
association with neurological subtle signs does verbal/ performance/full-scale IQ, spelling,
not significantly differ between PDD and arithmetic and social adversity. Children with
ADHD-CT, compared to healthy children, ADHD-CT had worse SWM, an ability to gen-
although the magnitude of the difference for erate strategy and spatial span than anxiety dis-
ADHD-CT was large and for PDD was moderate order, whether comorbid ‘anxiety’ was present
compared to primary school-age children with or not. Further, the children with ADHD-CT
anxiety disorders. and anxiety disorder, whether comorbid or not,
A third line of evidence supporting option performed the SWM task in the same way. As
(4) involves underlying cognitive risk factors. age increased, SWM ability improved in all
We extended our investigation of biological groups, although ADHD-CT had a worse SWM
risk factors associated with each condition by performance, whether anxiety disorder was
examining the association of anxiety disorders present or not. In contrast, children with
and ADHD and separately PDD and ADHD on ADHD-CT and PDD were indistinguishable on
a robust cognitive neuroscience construct, spa- their SWM performance and differed in their
tial WM. Of particular interest is whether approach to completing the SWM task: the
comorbid anxiety disorder differs from comor- ADHD-CT group relied on spatial span and
bid PDD in its effects on SWM performance strategy while the PDD group depended on
and the putative prefrontal cortical neural net- strategy alone. As age increased, SWM ability
works known to subserve this measure. The improved in all groups, which remained unable
extant literature suggests that comorbid anxiety to be differentiated. Gomez et al. (2014) simi-
disorder should have an independent impairing larly found that as verbal and spatial WM
effect on SWM (Tannock et al., 1995; Vance increased in ADHD young people, there was an
et al., 2013), as does PDD (Franklin et al., increase in depressive disorders, not anxiety.
2010), separate from MDD. A total of 125 chil- In summary, current lines of evidence suggest
dren (aged 7–12 years) were identified using that comorbid anxiety disorders with ADHD may
the DSM-IV: ADHD-CT alone (N = 25), arise from common biological and/or cognitive
ADHD-CT and anxiety disorder(s) (N = 25), risk factors. Furthermore, their association may
anxiety disorder(s) alone (N = 25), ADHD-CT also arise from their separate association with a
and PDD (DSM-IV equivalent) (N = 25) and third disorder such as a depressive disorder. Of
PDD alone (N = 25). Anxiety disorders were course, there may be a myriad of additional bio-
defined as DSM-IV GAD, SAD, social phobia logical and psychosocial risk factors and further
(DSM-V equivalent SoAD) and SpPh mediating third disorders yet to be characterised.
(American Psychiatric Association, 1994), Such factors and disorders may affect the chil-
diagnosed through a semi-structured clinical dren’s response to medication and/or psychologi-
interview with the child’s parent(s) (Silverman cal treatments offered.
146 A. Vance et al.
DHD and the Clinical Presentation

A impulsive. Fears about moving from a low-threat,
of Anxiety Disorders easily managed environment, such as the home
living room, to perceived higher-threat environ-
Children with anxiety disorders and comorbid ments where there are many more novel cues and
ADHD manifest features of both disorders in a competing stimuli to manage and prioritise are a
variety of situations – mainly the home environ- particularly important form of anxiety. As noted
ment, the school classroom and the peer social above, such separation anxiety is especially
interactions. It remains unclear whether the fea- comorbid with ADHD-CT and may indeed
tures of anxiety disorders and/or ADHD are worsen with age and the degree of defiance
affected by the presence of the other. The (Cantwell & Baker, 1992; Vance, 2005).
Multimodal Treatment Study of Children with Furthermore, they may become a main driver for
ADHD (MTA) (Jensen et al., 2001; Newcorn school refusal behaviour as can social anxiety,
et al., 2001) data implied that inattention rather especially the fear of being critically appraised
than hyperactivity-impulsiveness characterised by peers and/or teachers and found wanting. This
children with ‘anxiety’ and ADHD and that this type of anxiety is especially crippling from late
group had lower teacher-rated impulsiveness childhood into adolescence when peer group
than children with ADHD and ODD/ interactions become normative for young people,
CD. However, subsequent observation of these aside from their family of origin. Together, these
children did not discern significant differences in forms of anxiety are associated with children
their inattention, motor overactivity and/or being more tentative about engaging with new
impulsiveness in the school environment (Abikoff situations, novel tasks, taking appropriate risks to
et al., 2002). Earlier studies were similarly incon- facilitate their learning and trying new things
clusive (Pliszka, 1992; Livingstone et al., 1990), repeatedly in order to consolidate their skills
and currently, there are no compelling explana- base.
tions for these inconclusive results. Core anxiety Less commonly, these children may have
disorder symptoms and separately ADHD symp- severe and frequent tantrums associated with
toms can be better in some individuals while severe mood lability and marked defiance that
worse in others with additional comorbid ODD can predispose them to developing early-onset
and/or CD symptoms. ADHD and anxiety disor- depressive disorders such as DD and/or MDD
ders may be similar to each other in presentation (Fonesca & Perrin, 2001). The exact mechanisms
via observation. Also, it may be harder to identify for these outbursts can be hard to uncover clini-
anxiety disorders in the presence of core ADHD cally without careful interview of multiple infor-
symptoms because of a clinician bias to focus mants and occasionally direct observation over a
preferentially on the latter. Certainly, different number of days in an inpatient setting. Similarly,
contexts affect the manifestations of both types panic attacks are relatively rare prepuberty and
of disorder. This is particularly pertinent for the tend to occur in older children and adolescents
anxiety disorders. once their cognitive capacities are sufficiently
Generalised anxiety disorder, SpPh, SAD and well developed. The younger the child with panic
SoAD are the most frequent anxiety disorders attacks, the more likely the presence of a depres-
comorbid with ADHD. Children’s worries about sive disorder (Fonesca & Perrin, 2001).
how well they are performing compared to their Acute stress disorder and post-traumatic stress
peers, how accurate they are, how quick they are, disorder are also relatively rare prepuberty.
checking for errors and repeated requests for However, there has been considerable debate in
reassurance are common, although the worries the health and welfare literature about the possi-
will vary depending on the child’s situation and bly different phenomenology and clinical presen-
context. Specific fears of the dark, particular tation of these disorders in younger patients.
strangers or dogs may occasionally motivate Nevertheless, both anxiety disorders and ADHD
avoidance behaviours that can be repetitively are known to worsen in the context of traumatic
life events, particularly when repeated and/or of In addition, there are three more specific fac-
chronic duration. tors that may be particularly important to identify
Perhaps one of the most challenging clinical in children with anxiety disorders and comorbid
decisions is separating anxiety symptoms from ADHD: First, it is known that children with
inattentive symptoms as the main driver for a ADHD and anxiety disorders have first-degree
given child’s presentation. Moreover, there are relatives with substantially increased rates of
children who manifest both equally. Usually on anxiety disorders although they have similar lev-
careful history, taking the child with a primary els of ADHD compared to children with ADHD
anxiety disorder will self-report a number of key alone (Biederman et al., 1991a). Importantly,
anxiety symptoms that complete the impairing anxiety disorders and ADHD appear to be trans-
pattern of symptoms of one or more of the anxi- mitted independently in families (Braaten et al.,
ety disorders above. ADHD inattentive symp- 2003). This suggests that the familial risk of anxi-
toms, with and without hyperactive-impulsive ety disorders is separate from that of ADHD. This
symptoms, may be present but will be less fre- adds more weight to models that predict that
quent, less severe and clearly linked to worsening anxiety disorders and ADHD are not directly
anxiety symptoms and better as they abate. In related but rather are associated through the pres-
contrast, the converse is true for a child manifest- ence of biological and/or psychosocial risk
ing primary ADHD (parent and teacher report) factor(s) and/or disorder(s) that they have in com-
with secondary, more fragmentary self-reported mon. Second, maternal anxiety, overprotective-
anxiety symptoms. However, when both are ness and the lack of positive parenting are
equally present, there is similar frequency, sever- associated with anxiety disorders comorbid with
ity and timing of onset of both. ADHD (Pfiffner & McBurnett, 2006). These
interpersonal factors emphasise the environmen-
tal contribution to the onset and progression of
ADHD and the Assessment anxiety disorders. Furthermore, they suggest key
of Anxiety Disorders targets for the effective treatment of anxiety dis-
orders. Third, antenatal maternal stress, espe-
When taking the history, there are a number of cially ‘anxiety’, is associated with increased rates
key factors to identify that increase the risk of of core ADHD-CT symptoms, ODD symptoms,
anxiety disorders and ADHD, separately: these CD symptoms, aggression, anxiety and depres-
include for ADHD, a positive family history of sive disorder symptoms and more difficult tem-
first-degree relatives with ADHD (Biederman perament during infancy (Huizink et al., 2004;
et al., 1990), maternal smoking during their O’Connor et al., 2003; Van den Bergh et al.,
child’s pregnancy (Linnet et al., 2003), perinatal 2005a). Indeed, it has been estimated that the risk
complications (e.g. birth hypoxia) (Ben Amor of anxiety disorders comorbid with ADHD dou-
et al., 2005) and a vulnerable temperament with bles if maternal anxiety levels are in the top 15%
high levels of motor activity, inattention and dis- (Van den Bergh et al., 2005b).
tractibility (Sheese et al., 2007). Similarly, for The key risk gestational phase appears to be
anxiety disorders, a positive family history of from 12 to 22 weeks during the pregnancy (Van
first-degree relatives with anxiety disorders, shy- den Bergh & Marcoen, 2004): a time of peak
ness and behavioural inhibition in infancy neuronal migration, proliferation and differentia-
increased frequency of adverse life events across tion (Nowakowski & Hayes, 2002). This would
developmental life stages and social adversity necessarily contribute to aberrant prefrontal cor-
(e.g. multiple parental relationship breakdowns) tical, basal ganglia, medial temporal lobe and
(Leech et al., 2006; Phillips et al., 2005). Such parietal lobe neural network formation. These
factors form nonspecific risks for ADHD and anomalous neural networks are known to sub-
anxiety disorders, amongst other internalising serve working memory, response inhibition,
and externalising disorders. mood and arousal regulation difficulties
148 A. Vance et al.
associated with both anxiety disorders (lesser academic literacy and numeracy tasks and the
extent) and ADHD (greater extent) (Vance et al., interpersonal cues involved in making and keep-
2006, 2007). Possible mechanisms by which ing friends require considerable working mem-
antenatal maternal anxiety may contribute to ory processing and strategising resources. These
such neural network dysfunction include (1) vul- resources may be habitually, continually and pro-
nerability gene by environment interaction, (2) gressively more overwhelmed as these children
enhanced maternal hypothalamic- pituitary-move from one developmental stage to the next.
adrenal (HPA) axis function (hypercortisolae- Further, these theoretical models suggest clear
mia) leading to alterations in the foetal HPA axis medication and/or psychological treatments that
that influences the developing foetal brain and (3) may aid children with comorbid anxiety disor-
alterations in foetal blood flow affecting circula- ders and ADHD.
tion in the developing foetal brain (Sjostrom
et al., 2002; Talge et al., 2007). Regardless of
these possible mechanisms, this increased ante- ADHD and the Treatment of Anxiety
natal maternal anxiety along with paternal anxi- Disorders
ety and parenting style is an important target for
psychological and/or medication intervention. There are a variety of psychological and/or medi-
Examination of the child with comorbid anxi- cation treatment options available for children
ety disorders and ADHD should involve assess- with comorbid anxiety disorders and ADHD that
ment of cognition. There is emerging evidence have been shown to be effective. These include
that children with comorbid ‘anxiety’ and ADHD cognitive-behavioural therapy (CBT) and medi-
are impaired in their performance of cognitive cation options (Jensen et al., 2002; Pliszka, 2011;
tasks that require progressively more short-term Houghton et al., 2017; Silverman & Berman,
memory and working memory (Tannock et al., 2001). CBT includes response prevention, mood
1995). It remains unclear which specific anxiety and arousal regulation, social skills training and
disorders may be associated with this impairment desensitisation techniques, parent management
and whether there are other types of ‘anxiety’ training and educational school-based interven-
that enhance performance. In contrast, tasks that tions. To date, key issues remain such as whether
are focussed on reaction time with minimal work- ADHD affects the response of children with anx-
ing memory demands are usually performed bet- iety disorders to CBT with or without selective
ter by this comorbid group (Pliszka, 1992). This serotonin reuptake inhibitors (SSRIs), whether
pattern of results may be due to a modicum of anxiety disorders affect the response of children
increased anxiety leading to an increased alloca- with ADHD to stimulant medication, whether
tion of working memory processing resources ADHD medication treatment also helps anxiety
and alternative strategies within working mem- disorders, whether the psychological and/or med-
ory that are overwhelmed by tasks requiring large ication treatment of anxiety disorders helps
working memory reserves (Eysenck et al., 2007). ADHD and whether an optimal treatment algo-
Levy (2004) articulated a succinct neurophysio- rithm can be formulated for the treatment of anxi-
logical model to explain such findings: altered ety disorders comorbid with ADHD. In this
tonic/phasic dopaminergic firing in mesolimbic section, each of these key issues is addressed.
systems drives core ADHD symptoms while There is an inconsistent literature that notes
impaired prefrontal cortical and hippocampal the variable effect of ADHD and its treatment on
gating of amygdala-linked fear ‘anxiety’ activity the response of children with anxiety disorders to
at the level of the nucleus accumbens drives ‘anx- CBT (Pliszka, 2019). In addition, this same vari-
iety’. Both these theories help explain the aca- able effect of ADHD and its treatment has been
demic underachievement and social difficulties reported in children with anxiety disorders
these children experience that exacerbates their treated with SSRI medication (Faraone, 2018).
low self-esteem and ‘giving up’ attitude. Both At present, it remains unclear how comorbid
ADHD is exerting this variable treatment effect. cognitive deficits, such as impaired working
Possible mechanisms include the increased diffi- memory, are important because they contribute to
culty of children with ADHD developing insight educational underachievement as well as social
into their situation in life; inhibiting their skills difficulties, particularly the separate pro-
responses; planning, organising and prioritising cesses of making and keeping friends (Gathercole
their thoughts and actions; regulating their feel- & Alloway, 2006). Future systematic examina-
ings and mood; and controlling their level of tion of this issue is needed, particularly parsing
anxiety and/or aggression. In addition, children out specific anxiety disorders on their own versus
with ADHD tend to have a greater severity of being associated with an additional comorbid
associated anxiety disorder symptoms. disorder such as a depressive disorder [MDD,
Interestingly, Bloch et al. (2017) noted that stim- PDD] that has an independent separate effect on
ulant medication may decrease state anxiety in these cognitive functions (Vance, 2005, 2007). In
adults with ADHD and anxiety, along with fact, it is crucial to not ‘miss’ anxiety disorders
improving their core ADHD symptoms. Future associated with an early-onset depressive disor-
systematic investigation of these potential path- der such as PDD and/or MDD comorbid with
ways is needed. ADHD: such a depressive disorder may affect the
A number of early studies suggested that chil- patient’s response to the medication and/or psy-
dren with ADHD and comorbid anxiety disorders chological treatment provided (Vance, 2007). For
had an attenuated response to stimulant medica- example, there is evidence that the presence of a
tion and experienced more adverse effects, par- depressive disorder can be associated with an
ticularly autonomic adverse effects such as attenuated response of core ADHD symptoms to
stomach ache, headache, nausea, dysphoria and stimulant medication through increased prefron-
irritability (Buitelaar et al., 1995; Pliszka, 1989; tal cortical neural network dysfunction (Faraone,
Taylor et al., 1987). However, recent controlled 2018; Vance, 2007). Similarly, there is evidence
investigations have suggested that core ADHD that increased depressive disorder symptoms can
symptoms improve regardless of the presence of decrease the responsiveness to CBT, whether
anxiety disorders and that approximately 20% of ADHD is comorbid or not (Ewbank et al., 2020).
patients have significantly improved ‘anxiety’ Atomoxetine, a selective noradrenaline reup-
symptoms (Abikoff et al., 2005; Diamond et al., take inhibitor, may be helpful for decreasing
1999). The MTA (Jensen et al., 2001; The MTG ADHD, anxiety and depressive symptoms, when
Cooperative Group, 1999) study data revealed these conditions occur together (Stock et al.,
that the ADHD and ‘anxiety’ group responded to 2001). However, more controlled trials focussed
the psychological intervention alone arm, while on again separating anxiety disorders from
the ADHD alone and ADHD and comorbid ODD/ comorbid DD and/or MDD are needed (Vance,
CD groups did not. They also required a lower 2007). In contrast, there is ample evidence sup-
dose of stimulant medication and optimally porting the effectiveness of selective serotonin
responded to both stimulant medication and psy- reuptake inhibitors (SSRIs) for a range of anxiety
chological treatment together. Interestingly, the and depressive disorders (Geller et al., 2007).
comorbid ADHD and ‘anxiety’ and ODD/CD Interestingly, to date, there is not compelling evi-
group required combined medication and psy- dence that the SSRIs in association with stimu-
chological treatment, while medication alone lant medication improve comorbid anxiety
was sufficient for the ADHD alone and ADHD symptoms while the core ADHD symptoms are
and ODD/CD groups. Adverse effects were not improved by stimulant medication, regardless
increased in this comorbid anxiety disorders and (Abikoff et al., 2005). Similarly, a recent trial of
ADHD group. SSRIs and atomoxetine in this comorbid group
The response of cognitive deficits associated revealed that core ADHD symptoms alone
with ADHD to stimulant medication when anxi- improved (Kratochvil et al., 2005). There are no
ety disorders are evident remains unclear. These controlled trials of other key third-line
150 A. Vance et al.
edications for ADHD such as clonidine, imip-

m both disorders need specific, targeted treatment.
ramine or risperidone. However, there are pub- Multi-informant reports are imperative because
lished case reports (Huffman & Stern, 2007) parents and teachers are better at identifying
combined with clinical experience that allow externalising problems such as ADHD while
some further pertinent observations: Clonidine, a children are best at revealing anxiety and depres-
central noradrenergic agonist that decreases the sive problems that are affecting their lives at
functional level of activity of the noradrenaline home, in the school classroom and in the school
system, has been shown to decrease the core playground. Detailed symptom patterns of differ-
symptoms of ADHD. There may be a subset of ent anxiety disorders are needed, especially as
children with anxiety disorders comorbid with the clinical research fields begin to work out
ADHD that also gain benefit for their anxiety which anxiety disorders confer risk and which
symptoms because of this reduced noradrenaline anxiety disorders may be helpful for comorbid
drive. Imipramine is remarkably similar to atom- ADHD symptom domains and associated cogni-
oxetine in its pharmacodynamic and pharmacoki- tive deficits such as working memory. Also, pos-
netic effects, apart from its potential cardiotoxic sible third disorders, like PDD and/or MDD,
(conduction anomaly) adverse effects that atom- exerting an effect on the relationship of anxiety
oxetine does not share but clonidine does. disorders with ADHD need to be carefully and
Imipramine has known benefits for anxiety and systematically uncovered and treated if children’s
depressive disorder symptoms along with core response to treatment is to be optimised.
ADHD symptoms. However, because of potential Structured clinical interviews and parent, teacher
cardiotoxic effects, imipramine and clonidine and child questionnaires can be very helpful and
should only be used by specialist psychopharma- efficient ways of obtaining this information.
cology units and practitioners after a thorough Details of family history, particularly of anxiety
assessment that includes a cardiac history and disorders in first-degree relatives, maternal ante-
examination and an electrocardiogram prior to natal stress and family overprotectiveness and the
using these medications (Vance, 2008). lack of positive parenting practices are especially
Risperidone, an atypical neuroleptic medication relevant for comorbid anxiety disorders and
with particular dopamine (D2) and serotonin ADHD. Finally, overt signs of physiological anx-
(5HT2) receptor blockade effects, helps reduce iety need to be noted such as motor tension, rest-
anxiety and depressive symptoms and core lessness, autonomic arousal (including dilated
ADHD symptoms, particularly in low dose for pupils, sweating and fine peripheral tremor),
children with autistic spectrum disorders and/or variations in speech volume and rate, emotional
intellectual disability. Again, because of its inflection and abnormal involuntary movements
potential motor adverse effects, especially tardive (including tics, mannerisms and stereotypies).
dyskinesia, risperidone should only be used by The first treatment issue is to ensure parent’s,
specialist psychopharmacology units and practi- child’s and teacher’s awareness of the comorbid
tioners (Vance, 2008). state and to emphasise that both anxiety disorders
and ADHD need specific and targeted treatment,
monitoring of treatment outcomes and clear
Chapter Summary ongoing prioritisation of psychological and/or
medication treatments depending on the child’s
There are a number of assessment and treatment and family’s response. A range of psychological
points that emerge from this overview of comor- treatments and/or medication treatments are
bid ADHD and childhood anxiety disorders: available, and the possible options should be dis-
Early recognition of the comorbid state is crucial cussed with each child and his/her parents, using
for many parents, teachers and children, them- a benefit/adverse effect/crisis plan/review plan
selves, who do not understand that they may have treatment planning model. The effects of treat-
anxiety disorders in addition to ADHD and that ment will vary from the home environment to the
school classroom and playground for both anxi- Beriault, M., Turgeon, L., Labrosse, M., Berthiaume, C.,
Verreault, M., & Godbout, R. (2018). Comorbidity
ety disorders and ADHD. Finally, the current lit- of ADHD and anxiety disorders in school-age chil-
erature suggests that specific, single psychological dren: Impact on sleep and response to a cognitive-
and medication interventions should be trialled behavioral treatment. Journal of Attention Disorders,
first and evaluated in each patient before combin- 22, 414–424.
Biederman, J., Faraone, S. V., & Keenan, K. (1990).
ing treatments. This is crucial to avoid potential Family genetic and psychosocial risk factors in DSM
adverse effects being augmented when benefits III ADHD. Journal of the American Academy of Child
remain modest. As the clinical research field and Adolescent Psychiatry, 29, 526–533.
matures, these potential psychological and medi- Biederman, J., Faraone, S. V., & Keenan, K. (1991a).
Familial associations between ADHD and anxiety dis-
cation treatment combinations will be continu- orders. American Journal of Psychiatry, 148, 251–256.
ally refined to ensure their optimal synergism. So Biederman, J., Faraone, S. V., & Mick, E. (1991b). Clinical
maximal developmental and functional outcomes correlates of ADHD in females: Findings from a large
for these children will be facilitated and achieved. group of girls ascertained from pediatric and psychiat-
ric referral sources. Journal of the American Academy
of Child and Adolescent Psychiatry, 38, 966–975.
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Comorbid and Secondary
Depression in Child 11
and Adolescent Anxiety
Robert W. Garvey, Michelle K. Hiner, Chris A. Kelly,

and Margaret S. Andover
A high rate of comorbidity between anxiety and omorbidity Among Specific

C
depressive disorders has been demonstrated in Anxiety Disorders
children, adolescent, and adult populations.
Among adults and youth with a primary depres- Although high rates of comorbidity between
sive disorder, comorbidity with anxiety is as high depressive and anxiety disorders have been well
as 75% (e.g., Lamers et al., 2011; Sørensen et al., documented, comorbidity varies in rate and pre-
2005), and among those with primary anxiety sentation across individual anxiety disorders.
disorders, comorbidity with depression is 81% Among patients with a primary anxiety disorder,
greater than expected by chance (e.g., Kovacs & comorbidity of depressive disorders is greatest
Devlin, 1998; Lamers et al., 2011). These rates with generalized anxiety disorder (GAD) and
have been reported in both community and clini- social anxiety disorder (SAD) and lowest with
cal samples of youth (e.g., Costello et al., 2003; separation anxiety disorder and agoraphobia (e.g.,
Sørensen et al., 2005). Moreover, studies may Lamers et al., 2011; Verduin & Kendall, 2003).
underreport due to a presumption of diagnostic Increasing evidence regarding variation in the pre-
stability within and between depressive and anxi- sentation and outcomes across individual anxiety
ety disorders (e.g., Oquendo et al., 2004; Scholten disorders has led to a distinction between anxiety
et al., 2016). In this chapter, we discuss issues disorders related to the emotion of fear (i.e., panic
pertinent to the understanding of comorbid anxi- or phobia) and those related to the emotion of anx-
ety and depression among children and iety (i.e., GAD; Krueger & Markon, 2006), includ-
adolescents. ing the associations between fear- and
anxiety-related disorders and familial major
R. W. Garvey · M. S. Andover (*) depressive disorder (MDD). Warner et al. (2008)
Department of Psychology, Fordham University, found that fear-related disorders, but not anxiety-
The Bronx, NY, USA related disorders, mediated the association
e-mail: andover@fordham.edu
between parental MDD and child
M. K. Hiner MDD. Nonfamilial MDD, however, is associated
The Bronx, NY, USA with both fear- and anxiety-related disorders.
These results support the distinction between fear-
School of Psychology and Counseling, Fairleigh
Dickinson University, Teaneck, NJ, USA and anxiety-related disorders in some children and
suggest that treating fear-related disorders in the
C. A. Kelly
Department of Psychiatry, Icahn School of Medicine children of depressed parents may help prevent the
at Mount Sinai, New York, NY, USA subsequent onset of depression. Li et al. (2012)
https://doi.org/10.1007/978-3-031-14080-8_11
158 R. W. Garvey et al.
demonstrated heterogeneity in the number of Newman, 2017). However, comorbidity may not
MDD diagnoses across various anxiety disorders; be best represented by any single model. This
specifically, GAD predicted early onset of MDD, nuanced, transdiagnostic landscape is representa-
while PD predicted the highest number of MDD tive of the inherent difficulties in identifying the
diagnostic criteria. Research that fails to attend to etiology, biomarkers, and treatments for all indi-
specific anxiety disorders may yield nonsignifi- vidual mental disorders, which may be best cap-
cant associations due to differences in associations tured by one General Psychopathology dimension
and the directionality of relationships. (p value) rather than the traditional higher-order
factors of internalizing, externalizing, and
thought disorder (e.g., Caspi et al., 2014). This p
epression Secondary to Anxiety
D factor is highly heritable, and increased levels of
Disorders p factor in childhood and adolescence predict
dysfunction and diagnosis of a psychiatric disor-
Research has shown the onset of anxiety disorders der in adulthood (Allegrini et al., 2020; Cervin
to generally precede the onset of depressive disor- et al., 2021). Thus, the development of a transdi-
ders in children and adolescents (e.g., Avenevoli agnostic model for comorbid anxiety and depres-
et al., 2001; Lamers et al., 2011; Starr et al., 2014)). sion may be representative of the approach
In studies of youth with comorbid anxiety and needed to refine psychiatric nosology and treat-
depression, the anxiety disorder preceded the ment more generally.
depressive disorder in two-thirds of cases (e.g.,
Seligman & Ollendick, 1998; Starr et al., 2014).
Risk of secondary depression is 2–4 times greater Tripartite Model
among adolescents with an anxiety disorder
(Wittchen et al., 2000), and the presence of anxiety Early models characterized anxiety and depres-
has longitudinally predicted depression in children sion as expressions of the same underlying pro-
and adolescents (e.g., Costello et al., (2003). cess included in the internalizing dimension and
Particular characteristics of anxiety disorders also comorbidity between the disorders representing
increase the risk of depression secondary to anxi- this single construct (Krueger & Markon, 2006).
ety. Specifically, depression secondary to anxiety As an alternate model, Clark and Watson’s (1991)
is positively associated with the number of comor- tripartite model of anxiety and depression recog-
bid anxiety disorders, severity of anxiety disorders nizes their shared and unique presentations.
at baseline, frequency of avoidance, and presence According to this model, anxiety and depression
of panic attacks (Bittner et al., 2004; Wittchen share high levels of negative affect, but while low
et al., 2000). However, research suggests that this positive affect is unique to depression, high phys-
temporal pattern may not be present for all anxiety iological arousal is unique to anxiety.
disorders. While individuals with SAD and GAD Longitudinal studies of adolescents show strong
are particularly at risk for the development of sub- support for a three-factor model, demonstrating
sequent depression (e.g., Bittner et al., 2004; that despite the presence of one underlying com-
Kessler et al., 2008; for an exception, see Avenevoli mon factor, factors specific to depression and
et al., 2001), onset of PD typically does not pre- anxiety account for the differences in symptom
cede depression (Avenevoli et al., 2001). presentation (Olino et al., 2008). However, some
have found high physiological arousal and nega-
tive affect to be the underlying factor (Anderson
Models of Comorbidity & Hope, 2008; Chorpita et al., 1998; Compas
et al., 2004), while others lend partial support to
Several models have been developed to explain the tripartite model (Jacques & Mash, 2004;
the relationship between anxiety and depression Ollendick et al., 2003). In addition, the tripartite
(e.g., Cummings et al., 2014; Jacobson & model does not perform similarly across anxiety
11 Comorbid and Secondary Depression in Child and Adolescent Anxiety 159
disorders. For example, negative affect is related toms increase the likelihood of intensified
to GAD as well as depression, and physiological depressive symptoms and the development of a
hyperarousal is more strongly associated with PD depressive disorder. Although the anxiety disor-
than other anxiety disorders (Anderson & Hope, der preceded the depressive disorder, depressive
2008). Even within a single anxiety disorder, pat- symptoms preceded anxiety symptoms.
terns of positive affect, negative affect, and phys- Jacobson and Newman (2017) propose a model
iological arousal have been found to differ in which anxiety and depression symptoms bidi-
between adolescents meeting diagnostic criteria rectionally predict one another in short- term
and those experiencing elevations in symptoms fluctuations until a threshold of symptom sever-
(Anderson et al., 2010). Consequently, the tripar- ity is met, resulting in risk for the development
tite model may best fit GAD-depression comor- of the other disorder. However, this model does
bidity, while alternative models may characterize not rule out the existence of additional contrib-
comorbidity among other anxiety disorders and uting variables (e.g., stress) and is based on only
depression. one study on the bidirectional longitudinal rela-
tionships between anxiety and depression symp-
toms and disorders. Additional research on the
Bidirectional Model longitudinal association and mechanisms of
anxiety and depression are needed to better
Findings of the strong temporal relationship assess the model’s validity.
between anxiety and depression suggest that the
presence of an anxiety disorder may actually be
a risk factor for depression (Hammen et al., Developmental Model
2008; Seligman & Ollendick, 1998; Wittchen
et al., 2000). The consequences of anxiety, such A growing body of evidence supports a develop-
as deficits in social and academic functioning, mental approach in accounting for the differ-
may be depressogenic factors that lead to the ences in the onset of anxiety and depression and
later development of a depressive disorder (e.g., examining how their relationship changes as a
Seligman & Ollendick, 1998). Avoidance, low function of time, rather than observing trends in
sociability, and interpersonal oversensitivity already developed comorbidity (e.g., Kovacs &
mediate later depressive disorders (Jacobson & Devlin, 1998; Rice et al., 2004). Olino et al.
Newman, 2014; Starr et al., 2014). However, in (2008) propose that the temporal relationship
a meta-analysis of the longitudinal relationship between anxiety and depression may be due to
between anxiety and depression, depression the presence of a common factor early in devel-
predicted some anxiety disorders to a greater opment (e.g., an internalizing factor; Fergusson
degree than did anxiety predict depression et al., 2006). Then, an anxiety-specific factor
(Jacobson & Newman, 2017). One possible presents early in development, with depression-
explanation for these contrary results lies in the specific and additional common factors develop-
examination of symptom onset rather than onset ing as the individual matures. For example,
of diagnosis, as the impact of comorbid anxiety negative affect, underlying both anxiety and
and depressive disorders may be in their effect depression, may present in early childhood, but
on the other’s symptoms (e.g., Bubier & children may be protected from depressive
Drabick, 2009). For example, a child may symptoms by positive affect until later in the
develop subthreshold depressive symptoms development when physiological and neurologi-
leading to the development of broad levels of cal maturation decreases the ability to experi-
avoidance and low behavioral activation. In ence reward and positive affect (e.g., Forbes
turn, newly developed anxiety symptoms are et al., 2009; Poletti, 2009). Alternatively, Kovacs
exacerbated to a level of chronicity needed for and Devlin (1998) propose that childhood anxi-
disorder diagnosis. Finally, the anxiety symp- ety may be a manifestation of developmental
maturation related to the psychophysiology of isk Factors for Comorbid

R
emotional dysregulation and associated psycho- Depression
pathology. They suggest that the younger a child
is, the more likely that the onset of such pathol- Various biological, psychological, and environ-
ogy will take the form of anxious symptoms. As mental factors have been implicated in the etiol-
such, comorbidity models emphasizing a single ogy of early-onset anxiety and depression. While
mixed factor may fit best for young children, research explicitly investigating comorbid anxi-
while two-factor models may be a better fit for ety and depression is limited, research investigat-
older children (Cannon & Weems, 2006; Cole ing anxiety or depression alone often contributes
et al., 1997). to an understanding of an underlying common
Cummings et al. (2014) propose a develop- etiology. In the following sections, we examine
mental model which maps depression comorbid- some of the specific factors involved in the etiol-
ity with specific anxiety disorders rather than as ogy of anxiety and depression that are also impli-
one homogenous group. The first of three path- cated in the comorbidity of the disorders.
ways is characterized by the development of
fear-related anxiety symptoms during childhood
(e.g., SAD), which, when untreated, become a Biological Risk Factors
risk factor for the development of depression
during adolescence (Cummings et al., 2014; Genetics Research Parental depression, comor-
Watson, 2005). The second pathway is indicative bid anxiety and depression, and primary anxiety
of children with anxiety-related disorders, dem- disorders have been strongly associated with an
onstrated to be distinct from fear-related anxiety increased genetic risk for comorbid anxiety and
disorders and associated with greater overlap depression in offspring (e.g., Micco et al., 2009;
between anxiety and depression (Warner et al., Guffanti et al., 2016). Family and twin studies
2008). This pathway most commonly manifests indicate at least a moderate influence of genes on
as depression-GAD comorbidity, marked by an risk for comorbid anxiety and depression in chil-
overlap of symptoms associated with worry, and dren, with studies finding much of the covariation
includes the most shared risk factors between of anxiety and depressive symptoms in child
anxiety and depression of any pathway twins due to a common genetic influence
(Cummings et al., 2014). Although onset of (Middeldorp et al., 2005). It should be noted,
depression and anxiety may occur simultane- however, that genetic effects for comorbidity
ously in this pathway, they may also onset sepa- may differentially affect children based on age.
rately due to age-related life events (Hyde et al., For example, the magnitude of genetic effects
2008). The third pathway is the least common may increase with age (Waszczuk et al., 2014),
form of anxiety-depression comorbidity, in and certain genetic vulnerabilities may only
which depressive impairment leads to the devel- become active post-puberty (Waszczuk et al.,
opment of anxiety secondary to impairment. 2016). Despite increased rates of comorbid anxi-
Depressive impairment has been linked to subse- ety and depression in adolescent females
quent anxiety (Rudolph et al., 1994) in older (Zavaglia & Bergeron, 2017), increased genetic
adolescents and adults, but additional research is liability does not appear to differentially affect
needed (Cummings et al., 2014). One advantage children based on sex (Trzaskowski et al., 2019).
of the multiple-pathways model is that it incor- For stand-alone disorders, parental anxiety disor-
porates alternative developmental models of der—especially PD and GAD—confers greater
comorbid anxiety and depression. Longitudinal risk for offspring anxiety and depressive
studies should continue to examine the develop- disorders, although the risk for offspring anxiety
mental trajectories of anxiety-disorder comor- disorders may be greater than for offspring
bidity among specific anxiety and depressive depressive disorders (Lawrence et al., 2019).
disorders. Further, specific anxiety disorders comorbid with
depression have different genetic risk profiles adversity in early childhood (Park et al., 2018)
(Kendler et al., 1995; Waszczuk et al., 2014). and may be a functional marker for increased
Genetic research also provides support for the vulnerability to the development of anxiety
temporal pattern of onset. Specifically, Eaves symptoms during the transition to adolescence
et al. (2003) found that genes that increased risk (Barendse et al., 2020). Imaging studies in youth
for childhood anxiety directly influenced the later MDD have implicated connectivity between the
development of depression. anterior cingulate cortex, the ventromedial pre-
frontal cortex, and the amygdala as predictive of
In twin studies, the shared environment influ- depressive illness markers including severity and
ences the development of anxiety symptoms and duration (Kerestes et al., 2014).
disorders and depression symptoms (Burt, 2009;
Ehringer et al., 2006; Thapar & McGuffin, 1997).
The nonshared environment has a small to mod- HPA Axis Research The amygdala, hippocam-
erate effect on the development of comorbid anx- pus, and prefrontal cortex are also involved in
iety and depression in children and adolescents hypothalamus-pituitary-adrenal (HPA) axis regu-
(Cerdá et al., 2010; Eley et al., 2015) and a mod- lation, which is implicated in both depression and
erate to large effect on most of the unique vari- anxiety (Juruena et al., 2020; Pariante &
ance of discrete anxiety and depressive disorders Lightman, 2008). Chronic stress-induced activa-
(Waszczuk et al., 2014). Genetic influence on tion of the HPA axis, which results in higher lev-
comorbid anxiety and depression is also influ- els of cortisol, can disrupt functioning in regions
enced by phenotypic heterogeneity and by heri- of the brain responsible for regulating emotion
table neurological and cognitive risk factors and therefore interfere with the ability to cope
(Ormel et al., 2019). effectively with stress. While depression specifi-
cally disrupts the HPA response to stress, anxiety
Neurobiology Research The amygdala and appears to be more relevant in noradrenergic dis-
hippocampus are implicated in fear, memory, and ruption. Thus, HPA disruptions in anxiety disor-
information processing (for a review on informa- ders may be due to the influence of comorbid
tion processing and risk for anxiety and depres- depression. While depression has been associated
sion symptoms in youth, see Lau & Waters, with HPA axis anomalies among children, only
2017). Anxious and depressed youth have been anxiety subscales, and not specific anxiety disor-
found to have smaller amygdalae than healthy ders themselves, have been associated with such
children (Merz et al., 2018; Strawn et al., 2015). anomalies (Adam, 2006; Chen et al., 2017;
Child and adolescent anxiety and depression are Kallen et al., 2008). Additional research on the
correlated with altered amygdala activation to role of the HPA axis is necessary, especially
negative information, although there may be dis- among children and adolescents specifically
tinct activation differences between the disorders (Lopez-Duran et al., 2009).
even when comorbidity is present (Beesdo et al.,
2009; Roberson-Nay et al., 2006). Studies indi-
cate decreased hippocampal volumes in child and Neurotransmitter Research All anxiety and
adolescent depression, even when accounting for depressive disorders are polygenic in nature, and
stressful life events, but the presence of comorbid few specific genetic loci have received consistent
anxiety appears to contribute no influence (Barch empirical support due in part to this broad under-
et al., 2019; McKinnon et al., 2009); however, lying vulnerability. Polymorphisms of the sero-
both reduced amygdala and hippocampal volume tonin transporter gene promoter (5-HTTLPR), in
have been found to be impacted by adversity interaction with stress, may increase risk for both
(Frodl et al., 2017; Weissman et al., 2020). anxiety and depression in adolescents, although
Functional connectivity between the amygdala particular alleles may confer different risks for
and the prefrontal cortex is impacted by increased comorbid anxiety and depression depending on
the developmental period and sex (Jenness et al., roticism rates are heterogenous across different
2011; Perry et al., 2017; Uher & McGuffin, anxiety disorders (Li et al., 2012).
2008). The allelic variants of 5-HTTLPR may
also be related to cognitive, psychological, and Interpretive Biases Interpretive biases, or falla-
neurological risk factors for comorbid anxiety cies in how people decipher ambiguous stimuli,
and depression, such as neuroticism, shyness, are a type of cognitive bias that bears a linear
behavioral inhibition, and amygdala activation relationship with the severity of depressive symp-
(Arbelle et al., 2003; Johnson et al., 2016; toms (Lee et al., 2016; Smith et al., 2018). Certain
Kruschwitz et al., 2015). However, candidate- types of interpretive biases have been implicated
gene approaches, like those used to identify the in anxiety disorders as well, showing a possible
5-HTTLPR polymorphism, have been criticized similarity in the cognitive mechanisms for anxi-
for failures to replicate. ety and depression. For example, catastrophizing
(i.e., anticipating the outcome of an experience
will be disastrous), personalizing (i.e., taking
Psychological Risk Factors inordinate personal responsibility for negative
events), and overgeneralizing (i.e., assuming that
Temperament and Personality Certain types the outcome of one experience will apply to simi-
of temperament, such as behaviorally inhibited lar experiences in the future) are more closely
and neurotic temperaments, may serve as vulner- associated with youth with anxiety disorders than
ability factors for the development of psychopa- those without (e.g., Cannon & Weems, 2010).
thology. Behavioral inhibition, marked by Additionally, these three subsets of interpretive
amplified sensitivity to novel stimuli and avoid- bias in particular are more strongly related to
ance of unfamiliar environments and people (Fox individuals with comorbid anxiety and depres-
et al., 2005; Henderson et al., 2015), is identifi- sion than to individuals with noncomorbid anxi-
able from infancy and is notably stable from early ety disorders or depressive disorders (Weeks
childhood into adulthood (e.g., Henderson et al., et al., 2017).
2015). Evidence suggests that behavioral inhibi-
tion is related to comorbid anxiety and depressive
disorders in youth and adults (Dougherty et al., Behavioral Processes Dysfunctional social
2013; Muris et al., 2011; Schofield et al., 2009; behaviors are common coping mechanisms in
Sportel et al., 2011). However, the relationship children with anxiety, although these behaviors
between behavioral inhibition and internalizing may cause or exacerbate secondary depression.
disorders may be influenced by multiple factors, For example, self-isolating from peers is fre-
including parenting style, attachment style, and quently seen in children with certain anxiety dis-
life experiences (Muris et al., 2011; Williams orders, especially SAD (Teo et al., 2013).
et al., 2009). Though avoiding social interaction may be a
protective behavior in anxiety, social isolation
A neurotic disposition, defined as the ten- may lead to feelings of loneliness, which can
dency to have negative affectivity, irrational trigger or worsen preexisting depressive symp-
ideas, and poor reactions to stressors, is also toms (e.g., Cohen & Wills, 1985). Although
related to anxiety and depression (e.g., Costa & avoidant behaviors may temporarily alleviate
McCrae, 1992; Moscati et al., 2016; Mathew anxiety, they mediate earlier anxiety and later
et al., 2011). Differences in neuroticism levels depression, indicating that evading anxiety-pro-
may explain between 20% and 45% of comorbid- voking situations may reduce social support that
ity between depressive and anxiety disorders, as acts as a preventative factor in depression
comorbidity is related to neurotic traits (Khan (Jacobson & Newman, 2014; Mathew et al.,
et al., 2005; Lamers et al., 2011). However, neu- 2011).
Seeking reassurance from others is another of perceived discrimination that members of sex-
strategy used often by children with some anxiety ual minority communities experience when com-
disorders, such as GAD and SAD (e.g., Beesdo- pared with heterosexual, cisgendered individuals
Baum et al.; 2012; Cougle et al., 2012). However, (Almeida et al., 2009).
excessive reassurance seeking is associated with
negative responses from others and can lead to Parental Psychopathology Parental psychopa-
interpersonal rejection, a factor that prospectively thology is among the most reliable and clinically
predicts depression (Nolan et al., 2003; Starr & salient risk factors for the development of inter-
Davila, 2008). nalizing problems and associated pathological
behavioral outcomes in children. Weissman
et al.’s (2016) 30-year longitudinal study found
Contextual Risk Factors that the likelihood of an individual developing
either an anxiety disorder or MDD in their life-
Demographic Variables Female sex is associ- times was three times as high in offspring of
ated with an increased likelihood of experiencing depressed parents as in offspring of nondepressed
internalizing disorders. Rates of anxiety and parents. This same study found that children of
depression are similar among boys and girls up depressed parents were at a tenfold risk of devel-
until the ages of 12–13 years, after which females oping prepubertal (i.e., early-onset) depression
begin to experience more anxiety and depressive when compared to children of nondepressed par-
symptoms than their male peers (Hankin et al., ents (Weissman et al., 2016).
2015; Letcher et al., 2012). By adulthood, rates
for anxiety disorders and MDD are 1.9 times However, because internalizing disorders are
higher and 1.7 times higher for females, respec- more common among females than males (e.g.,
tively (Baxter et al., 2014). This may be in part Mathew et al., 2011) and because the role of pri-
due to unique problems faced by females during mary caregiver has historically been concomitant
adolescence, such as an increased emphasis on almost exclusively with women (e.g., Ruiz &
body image (Slater & Tiggemann, 2010) or more Nicolás, 2018), much of the existing literature on
significant peer relationships (De Goede et al., this topic is focused on the psychopathology of
2009). Moreover, sex is one of the only notable birth mothers and how it relates to child outcome
demographic factors that consistently predicts (e.g., Goodman, 2020). Longitudinal research
both anxiety and depression. indicates that prenatal maternal depression is cor-
related with health outcomes (e.g., depression,
Sexual orientation and gender identity are anxiety, immune function) into young adulthood
additional salient risk factors for the development (Capron et al., 2015; Pearson et al., 2013; Plant
of depression. Girls who reported romantic and/ et al., 2016). Moreover, maternal depression is
or physical attraction to the same sex reported associated with increased heart rate and aug-
suicidal ideation at more than five times the level mented activity levels in utero (Kinsella & Monk,
as heterosexual girls, and boys reported it at more 2009), less positive affectivity in infancy (Aktar
than ten times the level as their straight male et al., 2019), less active regulation in early child-
peers (Almeida et al., 2009). Similarly, transgen- hood (Feng et al., 2007), and increased delinquent
der adolescents report anxiety and depression at behaviors in adolescence (Wickham et al., 2015).
2–3 times the rate of their cisgendered peers This shows a pervasive pattern of negative out-
(Reisner et al., 2015). By adulthood, more than comes in children across development and can
half of transgender individuals and more than likely be explained by a diathesis-stress model.
one-third of lesbian, gay, and bisexual individu- Moreover, children with comorbid MDD and anx-
als experience clinically significant depressive iety disorders report more familial dysfunction
symptoms (Kaniuka et al., 2019). These dispari- than children with pure anxiety despite nonsig-
ties are partially explained by the greater amounts nificant differences in maternal psychopathology,
indicating a need to examine paternal symptomol- documented and salient in both short- and long-
ogy and parenting styles in addition to maternal term outcomes. One in ten cases of MDD in
factors (O’Neil et al., 2010). Overall, these studies childhood and adolescence becomes chronic,
further support the critical need for early identifi- with comorbid anxiety as a key predictive factor
cation and intervention for this particularly vul- (Rey et al., 2015; Shatkin, 2015).
nerable population of at-risk offspring. Whereas comorbidity inherently confounds
and complicates evidence of etiology, comparing
Life Events Stressful life events have been noncomorbid and comorbid outcomes facilitates a
shown to have negative effects on the mental more comprehensive understanding of the com-
health of young children (e.g., Moscati et al., pounded effect of youth depression comorbid
2016). Specifically, common stressful life events with anxiety. However, research examining
within the family, such as the death of a grand- comorbid outcomes using DSM-5 criteria is
parent or frequent arguments between parents, scarce, as the DSM-5 has added new criteria for
are predictive of anxiety disorders later in life MDD with anxious distress (American
(e.g., Kessler et al., 2008; Platt et al., 2016). Psychological Association, 2013). This change in
Other stress-inducing life events in childhood, nosology addresses the overlap in symptomology
such as serious illness and witnessing violence, between MDD and anxiety, as well as the preva-
are predictive of depression symptoms later in lence of comorbid presentations. Literature using
life, though this relationship can be mediated by DSM-IV-TR criteria has found that children and
parental and social support (e.g., Elmore & adolescents with comorbid anxiety disorders and
Crouch, 2020; Eisman et al., 2015). depression exhibit outcome characteristic of, but
more severe than, those who experience nonco-
Trauma and abuse are also major predictors of morbid depression (Costello et al., 2003;
internalizing psychopathology; however, the Merikangas et al., 2003; Moffitt et al., 2007). For
impact of trauma is more salient in depressive example, Foley et al. (2006) examined proximal
disorders than anxiety disorders (Hovens et al., psychiatric risk factors for suicidality in youth
2012). Further, trauma in childhood is a strong and found that individuals with an MDD-GAD
predictor of the emergence of comorbid depres- comorbidity had the greatest suicide risk of any
sion and anxiety later in life (Hovens et al., 2010). pure or comorbid anxiety or depression diagnosis.
Individuals with comorbid presentations may also
exhibit more greater rates of chronic/multi-
Outcomes episodic presentations, physical and mental debil-
ity, suicidality, and poor treatment response to
Early-onset anxiety and depression are associ- medication and psychotherapy than those with
ated with an array of short-term and long-term noncomorbid anxiety or depression (e.g., Bijl &
negative outcomes. Studies focusing on the Ravelli, 2000; O’Neil et al., 2010; Rush et al.,
effects of noncomorbid early-onset anxiety have 2005). Findings such as these raise essential ques-
shown that in general, youth anxiety disorders— tions regarding the fundamental disparity between
particularly SAD and separation anxiety disor- the pure and comorbid forms of these disorders.
der—are associated with high levels of
impairment, including social dysfunction, school
avoidance, and academic failure (Shatkin, 2015). linical Implications of Comorbid
C
Likely because of the heterogeneous nature of Depression
anxiety disorders themselves, there have been
noted differences in the long-term outcomes of Assessment
individuals diagnosed with youth anxiety disor-
ders (Ginsburg et al., 2018). The adverse effects Neither anxiety nor depression is a unitary phe-
of early-onset depression, however, are better notype, thus complicating the assessment of
these disorders. Depression and anxiety invento- crossover effects leading to improvements in the
ries are highly correlated, demonstrating a lack of comorbid condition. In a meta-analysis of RCTs
discriminant validity in the measures and an (randomized controlled trials) measuring the
overlap in symptomatology (e.g., Kendall et al., effects of depression or anxiety treatments on
1992). For example, two frequently used assess- both constructs, Garber et al. (2016) found that
ment tools, the Kutcher Adolescent Depression treatments for depression led to improvement in
Scale and the Revised Children’s Manifest both depressive and anxiety symptoms, although
Anxiety Scale (RCMAS-2), have items assessing more significantly in depressive symptoms.
irritability, nervousness, concerns about being a Likewise, treatments for anxiety disorders
“good person,” sleep problems, somatic com- resulted in improvements of anxiety and depres-
plaints, and difficulties with concentration sion symptoms with greater improvement in anx-
(LeBlanc et al., 2002; Reynolds & Richmond, iety symptomology. However, those with more
2008). As researchers create new measures that severe anxiety may benefit from focusing specifi-
better discriminate between depression and anxi- cally on anxiety symptoms in treatment (Young
ety, difficulties in doing so indicate the lack of et al., 2006).
specificity between disorders (Cox et al., 1999). Some studies have shown that comorbid anxi-
Belzer and Schneier (2004) make a series of ety disorders are associated with a poorer out-
recommendations regarding the assessment of come for depression treatment among children
comorbid anxiety and depression in adult and adolescents (Ollendick et al., 2008; Young
patients, saying clinicians should: (1) ask patients et al., 2006). This, in combination with the lower
with symptoms of depression about anxiety- efficacy of the primary treatment on the comor-
related symptoms, (2) inquire about age of onset bid condition, highlights the need for treatments
and whether any life events that act as risk factors to purposefully target comorbid disorders. Chu
accompanied the first symptoms, (3) discuss the et al. (2012) suggest three pathways of treatment
patients’ beliefs regarding the etiology of their for comorbid anxiety and depression: (1) flexible
symptoms (e.g., if their anxiety occurs only dur- single-target interventions, (2) modular-based
ing depressive episodes), and (4) discuss interventions, and (3) transdiagnostic interven-
responses to prior treatment. While these recom- tions. For example, patients with a great degree
mendations are in reference to adults, they are of symptom overlap may benefit from a transdi-
useful in child and adolescent populations. agnostic approach, while those with a primary
depressive disorder may benefit from a flexible
implementation of a depression treatment,
Treatment including the use of cognitive-behavioral princi-
ples to address anxious thoughts/distortions
As discussed above, youth with comorbid anxi- linked to depressive impairment.
ety and depression often experience more severe
symptomology and deficits in functioning than
youth with only one disorder. However, closely Conclusions
related risk factors for anxiety and depression
suggest that treatments addressing both disorders Comorbid depression presents unique chal-
simultaneously are more likely to use the same lenges to the understanding, assessment, and
mechanism of action and be more efficacious treatment of anxiety in children and adolescents.
(Garber et al., 2016; Garber & Weersing, 2010). Youth with comorbid anxiety and depression
Therefore, treatment of comorbid anxiety and experience more severe symptoms of depression
depression among youth should be considered than those with depression alone, and comor-
when either diagnosis is present. bidity may be associated with a life-course of
Nontransdiagnostic treatments targeting either psychopathology. While research has consis-
anxiety or depressive disorders demonstrate tently demonstrated that the onset of anxiety
precedes that of depression, the exact relation- Arbelle, S., Benjamin, J., Golin, M., Kremer, I., Belmaker,
R. H., & Ebstein, R. P. (2003). Relation of shyness in
ship between anxiety and depression is uncer- grade school children to the genotype for the long form
tain. Further, the effect of the interactions of of the serotonin transporter promoter region polymor-
different biological, psychological, and environ- phism. American Journal of Psychiatry, 160(4), 671–
mental risk factors over time on the develop- 676. https://doi.org/10.1176/appi.ajp.160.4.671
Avenevoli, S., Stolar, M., Li, J., Dierker, L., & Ries
mental trajectories of comorbid anxiety and Merikangas, K. (2001). Comorbidity of depres-
depression should be considered. Although sion in children and adolescents: Models and evi-
treatment of one disorder can be effective in dence from a prospective high-risk family study.
improving the symptoms of the comorbid disor- Biological Psychiatry, 49(12), 1071–1081. https://doi.
org/10.1016/s0006-3223(01)01142-8
der, interventions may be tailored to address Barch, D. M., Tillman, R., Kelly, D., Whalen, D., Gilbert,
comorbid anxiety and depression. Given the K., & Luby, J. L. (2019). Hippocampal volume
high rates of comorbidity among children and and depression among young children. Psychiatry
adolescence and the associated negative out- Research: Neuroimaging, 288, 21–28. https://doi.
org/10.1016/j.pscychresns.2019.04.012
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ranted in research and clinical work. Byrne, M. L., Seal, M. L., et al. (2020). Adrenarcheal
timing longitudinally predicts anxiety symptoms
via amygdala connectivity during emotion process-
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The Role of Disgust in Childhood
Anxiety Disorders 12
Ana Rabasco and Dean McKay
There has been extensive research into the role of in several influential theories and accounts of
disgust in a wide range of psychopathologies emotion (e.g., Darwin (1872/1998), Ekman
(e.g., Olatunji and McKay (2007), Schienle et al. (1992, 1999)), the disease-avoidance and social
(2003a)). Most of this research has focused on functions ascribed to disgust (Keltner & Haidt,
anxiety disorders where disgust may figure prom- 2001; Matchett & Davey, 1991), and the growing
inently in avoidance. The early work in this area appreciation for the role of disgust in adult psy-
focused on specific phobias and avoidance of con- chopathology (Olantunji et al., 2010; Olatunji &
tact with disease and contagion (Matchett & McKay, 2009), it was only after the publication
Davey, 1991). Since that time, the range and of Matchett and Davey’s (1991) disease-
nature of disgust’s involvement in psychopathol- avoidance model that researchers began to recog-
ogy have become refined and include a multifac- nize the pertinence of disgust to anxiety disorders
eted conceptualization drawing on the postulates and their treatment. The field has since witnessed
of the emotion as described by Rozin and Fallon a significant increase in the number of articles
(1987). This chapter focuses on the conjoint roles and book chapters published specifically address-
of disgust and development in childhood anxiety. ing the role of disgust in the phenomenology and
maintenance of anxiety disorders and other con-
ditions characterized by avoidance behaviors.
he Role of Disgust
T This is especially true of contamination-related
in the Maintenance of Avoidance obsessive-compulsive disorder (OCD) (e.g.,
Behaviors Berlin et al. (2017), Moretz and McKay (2008),
Olatunji et al. (2004), Tolin et al. (2006)), animal
Disgust has been described as “the forgotten phobias (e.g., de Jong et al. (1997), Matchett and
emotion of psychiatry” (Phillips et al., 1998), a Davey (1991), Polák et al. (2020)), and blood-
description that, until recently, was far from injection-injury (BII) phobia (e.g., Bianchi and
unwarranted. Despite the central role of disgust Carter (2012), Olatunji et al. (2006), Sawchuk
et al. (2002)).
While it appears that there is considerable
A. Rabasco support for the role of disgust in anxiety disor-
Fordham University, Bronx, NY, USA
ders, the majority of this research has focused on
D. McKay (*) adults. Nonetheless, the limited research that has
Bronx, NY, USA investigated the role of disgust in childhood anx-
e-mail: mckay@fordham.edu iety disorders is promising and seems to resem-
https://doi.org/10.1007/978-3-031-14080-8_12
174 A. Rabasco and D. McKay
ble the findings from the adult literature. The moral transgressions (Keltner & Haidt, 2001;
aim of this chapter is to summarize the major Rozin et al., 2004, 2009).
findings for the role of disgust in specific anxiety A closer inspection of the disgust state reveals
disorders, including the extant literature detail- a topography that distinguishes disgust from
ing this relationship in children. Where literature other basic emotions, such as fear, anger, guilt,
is limited or absent, we will provide predictions sadness, and joy (Ekman, 1999). The first defin-
and directions for future research in the area. ing component of disgust lies in its eliciting stim-
The following section provides an overview of uli. Disgust is elicited by stimuli that have the
disgust in general and its impact on psychopa- potential to contaminate (Rozin & Fallon, 1987).
thology. First, disgust will be defined and essen- Disgust elicitors are well known to many as a
tial theoretical issues presented. Second, the result of socialization and include stimuli such as
assessment of disgust in children and its rela- spoiled, dirtied, or socially unacceptable food
tionship with anxiety disorders will be (e.g., moldy yogurt, monkey meat, food that is
discussed. infested with cockroaches, ketchup on ice cream),
body envelope violations (e.g., mutilated or miss-
ing body parts, exposed innards, sores, deep
Disgust Defined wounds), body products (e.g., feces, urine,
mucus, vomit), death and dead bodies (e.g., rot-
Disgust has been defined as an emotion charac- ting corpses, graveyards, ashes of a cremated per-
terized by “a feeling of revulsion or profound dis- son), animals (e.g., maggots, cockroaches, flies,
approval aroused by something unpleasant or rats), sexual behaviors that may be considered
offensive” (Lindberg et al., 2002, p. 389). Rozin unacceptable within specific cultural groups
and Fallon (1987) provided a detailed theoretical (e.g., sex with animals, incest), poor hygiene
account that describes how disgust may operate (e.g., body odor, dirt under fingernails, greasy
both behaviorally and cognitively. According to hair, sticky hands), and general violations of
their definition, disgust is “revulsion at the pros- social and moral norms (e.g., cruelty, bad man-
pect of (oral) incorporation of an offensive object. ners, vulgarity (Haidt et al., 1994)). Although
The offensive objects are contaminants; that is, if there are some cross-cultural differences with
they even briefly contact an acceptable food, they regard to the kinds of stimuli that people find dis-
tend to render that food unacceptable” (p. 23). gusting, these seven domains of disgust elicitors
Both of these definitions adequately capture the appear to be consistent across cultures (Olatunji
fundamental essence of disgust, namely, the feel- et al., 2009). Furthermore, evidence of disgust
ing of repugnance or intense aversion that is trig- reactions in response to some human disgust elic-
gered by exposure to a distasteful or offensive itors (e.g., contaminated food) has been found in
object or situation. Disgust sensitivity is the trait- nonhuman great apes, although their response is
like predisposition of a person to become dis- muted (Case et al., 2020).
gusted in response to a particular group of stimuli, Disgust is also unique on the basis of its dis-
known as disgust elicitors (Woody & Teachman, tinctive facial expression (Cisler et al., 2009;
2000). Ekman, 1999). Izard (1977) described the typical
Disgust is conceptualized as a universally disgust facial expression as looking as if “one is
experienced emotion that was evolutionarily gagging or spitting out” (p. 336). Specifically,
selected to help humans solve a specific recurring when disgusted people typically open their
threat to survival via avoidance of contamination mouth, raise their upper lip, and wrinkle their
(Oaten et al., 2009). Over time, disgust has come nose. The tongue may also be protruding. The
to serve additional adaptive functions, such as person may lower his or her eyebrows and squint
defending against ideological contagions, regu- his or her eyes as a result of drawing up the nose
lating relations between social groups, safeguard- and upper lip (Izard, 1971). It has been shown
ing social order, and protecting the soul from that there is cross-cultural agreement in
12 The Role of Disgust in Childhood Anxiety Disorders 175
recognition of the disgust facial expression related information is often biased by the law of
(Ekman & Friesen, 1986; Izard, 1971), which contagion (Rozin et al., 1986), which states that
indicates that it is likely a universal human objects pass on some of their properties when
expression. This facial expression is found across they touch other things in such a way that the
cultures (Ekman, 1999) and in human infants effect of contact is sustained even after the con-
when administered bitter tasting substances nection has been broken (i.e., “once in contact,
(Steiner, 1979). always in contact” [p. 703]). For example, a
In addition to its unique facial expression, dis- patient may avoid touching an object that he fears
gust is characterized by unique autonomic ner- to be contaminated prior to entering his own bed-
vous system activity (Cisler et al., 2009; Ekman, room out of fear that his hand will contaminate
1999; Vrana, 2009). Physiological studies have his room, which he considers to be a contaminant-
consistently indicated a heart rate deceleration free “safe haven.” The processing of disgust-
for disgusting compared to fear-inducing and related material also has a propensity to be biased
neutral stimuli (see Cisler et al. (2009), Vrana by the law of similarity (Rozin et al., 1986).
(2009)). This is likely reflective of activation of According to this law, if a neutral stimulus
the parasympathetic nervous system (Page, resembles a disgusting stimulus, there is a greater
1994). In contrast, disgust imagery has been likelihood that it too will be perceived as being
found to increase heart rate (Vrana, 1993, 1994). disgusting (i.e., “the image equals the object”
McKay and Tsao (2005) offered an explanation [Rozin et al., 1986, p.703]). For example, people
for this apparent inconsistency. According to may refuse to consume chocolate that is shaped
these authors, imagery “may better address antic- like dog feces.
ipatory reactions. In this case participants may The cognitive processing of disgust-relevant
label the anticipatory reaction as anxiety, leading information seems to differ from that of other
to sympathetic activation, while live exposure emotions (e.g., fear) on the basis of primary dis-
more likely produces the diphasic reaction, with gust appraisals. Applying Salkovskis’ (1985)
parasympathetic arousal then occurring as well” model of OCD-related appraisals to disgust,
(p. 356). Similar to other negatively valenced Teachman (2006) differentiated between primary
emotions, disgust has also been linked to an aug- and secondary appraisals. In contrast to second-
mentation in the magnitude of startle reflex upon ary appraisals, which have to do with the conse-
presentation of disgust pictures, an increase in quences of becoming disgusted, Teachman
corrugator supercilii EMG (electromyographic) posited that primary disgust appraisals reflect
activity, and increased skin conductance (Vrana, beliefs about the properties of a stimulus (e.g.,
2009). Finally, there has been some neural cir- “blood and guts are disgusting”) or the likelihood
cuitry research suggesting projections from the of feeling disgusted (e.g., “if I look at the screen,
insula to regions controlling fear response (i.e., I will feel sick”). Thus, the content of primary
Schienle et al. (2017)), further supporting a role disgust appraisals is thought to be related to dis-
for disgust in anxiety reactions. gust or contamination, while the content of pri-
Disgust can also be set apart from other emo- mary fear appraisals is believed to be related to
tions on the basis of associated cognitive phe- danger (Woody & Teachman, 2000). Lastly, it
nomena (Cisler et al., 2009; Ekman, 1999; appears that the cognitive landscape of disgust
Teachman, 2006; Williams et al., 2009; Woody & may be characterized by unique attention, per-
Teachman, 2000). Central to this is the transfer- ceptual, and memory biases. If this is the case,
ability of disgust via the laws of sympathetic then these biases may have important implica-
magic. The two laws of sympathetic magic shape tions for the treatment and maintenance of
the circumstances under which people may per- disgust-related disorders. For example, Charash
ceive an unrealistic threat of contamination when and McKay (2009) have shown that individuals
there is no actual danger of becoming contami- with elevated contamination fear showed a bias
nated. First, the cognitive processing of disgust- in interpretation for vague situations that could
be associated with disgust, but not attention or stances that usually results in behavioral
biases for memory. Recent analyses have also avoidance. Even the facial expression of disgust
shown that disgust biases are more consistent can function as a natural mechanism in the behav-
than fear biases and that disgust facilitates recog- ioral immune system. For example, the function
nition of otherwise phobic stimuli (Wiens et al., of the disgust facial expression is to reduce the
2008). Williams et al. (2009) provide a detailed amount of offensive odor coming in through the
discussion of cognitive biases associated with nostrils and to expel the possibly hazardous con-
disgust. tents of the mouth after something distasteful has
Finally, the action tendency associated with been eaten or to serve as a barrier to ingestion in
disgust is behavioral avoidance (Ekman, 1999), a the first place. In addition to the facial expres-
characteristic shared with fear and anxiety. sion, neurovegetative components have also been
Similar to fear-based avoidance, the disgust reac- identified as part of the disgust reaction, specifi-
tion is characterized by the avoidance of objects cally an increase in saliva production and the ten-
or situations determined to be upsetting or dis- dency to vomit (Angyal, 1941). The extra saliva
turbing (Woody & Teachman, 2000). For exam- serves to dilute the offensive taste in the mouth
ple, an adolescent who is easily disgusted by and the nausea and vomiting function to avoid the
spoiled foods would theoretically be more likely ingestion of offensive objects. Physiologically,
to avoid consuming buttermilk or blue cheese disgust is associated with parasympathetic ner-
than would a disgust-insensitive child. Similarly, vous system activation. Recently, Stark et al.
a child who finds body envelope violations to be (2005) found that participants experienced a
objectionable might avoid looking at television decrease in heart rate and an increase in skin con-
shows depicting surgery. However, fear- and ductance response while viewing disgusting pic-
disgust-related avoidances are conceptualized as tures. Thus, Tomkins (1982) described disgust as
serving different functions. In contrast to fear- an “innate defensive response” (p. 377).
related avoidance, which is believed to have
served the function of distancing humans and
other organisms from imminent threats to physi- isease Avoidance and Animal
D
cal survival (Barlow, 2002; LeDoux, 1996), Phobias
disgust-related avoidance is theorized to have
aided by distancing humans from potential con- Matchett and Davey (1991) proposed that there
taminants (Keltner & Haidt, 2001; Matchett & was a connection between disgust and animal
Davey, 1991). phobia, known as the disease-avoidance model.
These researchers suggested that fear of some
animals is mediated by disgust sensitivity, as
he Disease-Avoidance Model
T opposed to being mediated by the threat of being
of Disgust attacked or physically injured. In other words,
individuals fear and avoid relatively harmless
The aforementioned characteristic facial expres- animals because these creatures are theoretically
sion of disgust is strongly connected to the connected to disease and contamination and
behavioral immune system. The behavioral therefore evoke feelings of disgust (e.g., rats,
immune system involves a series of psychologi- cockroaches, and spiders). As evidence, Matchett
cal mechanisms that detect the presence of infec- and Davey found that measures of disgust sensi-
tious pathogens and trigger emotional, cognitive, tivity and contamination were significantly cor-
and behavioral responses, which are meant to related with measures of fear for “fear-relevant”
protect people from infection (Schaller & Park, (but typically harmless) animals (e.g., rats, cock-
2011). Disgust has been strongly associated with roaches, and spiders) and “disgust-relevant” ani-
the behavioral immune system, as it is an emo- mals (e.g., slugs, maggots, and frogs). These
tional response to potentially dangerous sub- measures of disgust and contamination were not
significantly correlated with fear of the predatory Greece. They concluded that hygiene-related
animals that are likely to physically harm a per- behaviors across cultures were consistently moti-
son (e.g., lions, tigers, and bears). vated by avoidance of contact with disease-
Webb and Davey (1992) utilized an experi- causing pathogens. Extrapolating from their
mental design to further explore the role of dis- hygiene-related research, Curtis and Biran asked
gust sensitivity in some animal phobias. After people in these different countries about objects
completing self-report measures of fear for sev- that elicited disgust and found that these disgust
eral types of animals (i.e., fear-relevant, disgust- elicitors fell into five categories, including (1)
relevant, and predatory animals, as described bodily excretions and body parts, (2) decayed
above), participants were subjected to one of and spoiled food, (3) particular animals and
three different experimental conditions. insects, (4) certain categories of “other people,”
Participants viewed one of the following: a fear- and (5) violations of morality and social norms.
inducing video depicting extreme violence, a These categories, in their opinion, provide sup-
disgust-inducing video of bloody surgery in a port for the role of disgust as a defense against
hospital, or a neutral video of outdoor landscapes. the spread of infectious disease. The disgust elic-
The participants’ animal fears were reassessed itors in the first three categories clearly have the
after viewing the video, and for each experimen- potential to harbor disease. However, the last two
tal condition, pairwise comparisons conducted are more loosely related. According to Curtis and
for change in fear scores between the different Biran, avoidance of contact with disgusting
types of animals. The results indicated that the “other” people (e.g., “Americans,” as one respon-
violent material significantly increased fear of dent indicated in Greece) may prevent exposure
predatory animals only, while exposure to the to pathogens to which a person may not be
disgusting video led to a significant increase in immune. These authors also proposed that avoid-
fear of the fear-relevant and disgust-relevant ani- ance of immoral people and acts “may serve to
mals only. promote the avoidance of social rather than phys-
Ware et al. (1994) confirmed through factor ical parasites” (p. 29). This theory adds partial
analysis that animal fears can be divided into two support to the theory that disgust functions to
distinct categories, which they labeled fear- drive people away from potential sources of
relevant and predatory. Ware et al. also found a infection.
significant correlation between disgust sensitivity
and fear-relevant animal phobias only with no Disease avoidance and Children With the
such correlation between disgust and predatory exception of facial expressions, most accepted
animal fears. Furthermore, individual differences indicators of disgust (i.e., aversions to body prod-
in disgust sensitivity accounted for a significant ucts) appear to be absent in very young children,
amount of variance in fear of animals in the fear- not developing until about 5 years of age (Rozin
relevant category (e.g., snakes, bats, and & Fallon, 1987). Although Darwin (1872) noted
spiders). that he “never saw disgust more plainly than on
the face of one of [his] infants at the age of 5
months, when, for the first time…a piece of ripe
isease Avoidance and Disgust
D cherry was put into his mouth,” he qualified this
Elicitors observation by adding that he “doubt[ed] whether
the child felt real disgust” (p. 261). While the
Curtis and Biran (2001) have also proposed a characteristic facial expression may be the same,
disease-avoidance theory of disgust based on there seems to be a difference between the dis-
extensive qualitative research on disgust elicitors taste expressed by an infant and the “real” dis-
in several different cultures, including Africa, gust, endowed with meaning, which adults
India, the Netherlands, the United Kingdom, and experience.
Although there is ample support for the dis- on the floor, the parent may throw away the food
ease avoidance model of disgust in adults, there and react with disgust by giving certain facial and
is little evidence that the same theory applies to vocal responses that are observed and learned by
children. It has been shown in several experimen- the child. In support of this theory, Repacholi
tal studies (Rozin et al., 1986; Stein et al., 1958) (1998) found that young infants ranging from 14
that very young children react positively to typi- to 18 months old showed aversion to items toward
cal disgusting odors, such as synthetic sweat and which an adult had responded with disgust (i.e.,
feces. Furthermore, children are even willing to made a disgust face and said, “Eww! I’ve found
taste objects that would be rejected by most something! Eww! I can see it! Eww!” [p. 1019]).
adults, such as realistic-looking dog excrement Additional research has found that disgust reac-
made from peanut butter and stinking cheese. tions and avoidance behaviors can be learned by
Although children begin to reject food at around children simply through observation of adults
age five, Rozin and Fallon (1987) suggested that (Askew et al., 2014; Reynolds & Askew, 2019).
children do not yet refuse food based on disgust For example, Askew et al. (2014) conducted two
as it relates to contamination. They proposed that experiments with children examining the effects
the relationship between food rejection and dis- of disgust observational learning on children’s
gust emerges around age eight as cognitive skills disgust and fear beliefs and avoidance prefer-
develop that allow children to make a connection ences for novel animals. They found that chil-
between an object being introduced to a sub- dren’s fear beliefs and avoidance preferences for
stance and then removed, leaving trace amounts animals increased after they saw them together
behind (e.g., the concept that a bug briefly dipped with adult faces expressing disgust.
into a cup of juice may leave “germs” behind).
Furthermore, in a study of 38 monozygotic (MZ)
and 34 same-sex dizygotic (DZ) twin pairs, Rozin Assessing Disgust
and Millman (1987) found that although the sib-
lings were similar in their food preferences and Disgust sensitivity is most often measured by
beliefs about disgust and contamination, there self-report. As the conceptualization of disgust
was not a significant genetic contribution to these has changed over time, the content of the self-
variables. Similarities in food preference and dis- report measures has also changed accordingly.
gust sensitivity were therefore contributed to by An early self-report assessment was the Disgust
the shared family environment. Sensitivity Questionnaire (DSQ; Rozin et al.,
1984), a measure of disgust that addresses only
Development of Disgust Evaluative condition- one specific aspect of disgust sensitivity, food
ing (EC; de Houwer et al., 2001) has been pro- contamination. There is a simplified version of
posed as a mechanism for the acquisition of the DSQ (Muris et al., 1999) for administration to
disgust (Schienle et al., 2001). Evaluative condi- children. This simplified DSQ is comprised of 18
tioning is the process by which individuals learn items that ask how disgusting they would find it
to like or dislike an object based on its pairing to eat particular contaminated food items (e.g.,
with a positive or negative stimulus and a ver- “How disgusting would you find it to eat your
bally mediated label (de Houwer et al., 2001). favourite soup from a soup bow, after it had been
Oaten et al. (2009) recently reviewed the empiri- stirred by a thoroughly washed fly swatter?”
cal evidence supporting the disease avoidance “How disgusting would you find it to drink your
model of disgust and concluded that it is likely favourite lemonade, when a non-toxic leaf from a
that disease-related disgust develops in child- houseplant falls into your glass and goes to the
hood through EC via the pairing of disease- bottom?” and “How disgusting would you find it
related events with disgust reactions by their to eat your favourite cookie, after a bite had been
parents (e.g., parental facial expressions and ver- taken by a waiter in a restaurant?” (Muris et al.,
bal cues). For example, when a child drops food 2008b, p. 137)). Each item is rated on a five-point
Likert scale ranging from 1 (i.e., “not at all dis- Emotion Scale (DES) was designed to specifi-
gusting”) to 5 (i.e., “very much disgusting”), and cally measure disgust sensitivity. It consists of 30
the scores for all 18 items are summed to yield a items and assesses five domains of disgust: (1)
total score ranging from 18 to 90, with higher rotten foods, (2) small animals, (3) injections and
scores indicating increased disgust sensitivity. In blood draws, (4) mutilation and death, and (5)
a study of the connection between spider phobia smells. Participants are asked to rate their degree
and disgust sensitivity with young girls, de Jong of disgust using a five-point Likert scale.
et al. (1997) added two items to the original DSQ Research has shown that the DES total scale has
to assess spiders’ disgust-evoking status (i.e., excellent internal consistency (α = 0.91) and each
“How much would you like to eat your favourite subscale showed at least adequate internal con-
chocolate bar after a spider has walked across the sistency (rotting foods, α = 0.89; small animals,
bar when it is still wrapped in its package?” and α = 0.88; injections and blood draws, α = 0.58;
“How much would you like to eat your favourite mutilation and death, α = 0.84; and small ani-
chocolate bar after a spider has walked across the mals, α = 0.59 (Olatunji et al., 2007b)).
unpacked bar?” [p. 560]). The Disgust Propensity and Sensitivity Scale
A more comprehensive and widely used mea- (DPSS; Cavanagh & Davey, 2000) is a self-report
sure is the disgust scale (DS; Haidt et al., 1994). measure that assesses for both disgust sensitivity
The DS consists of 32 items measuring disgust and disgust propensity. Each item is rated on a
sensitivity among seven domains of disgust elici- scale from 1 (never) to 5 (always). The original
tors: food, animals, body products, sex, envelope DPSS measure consists of 32 items and has dem-
violations, death, and hygiene. There is an addi- onstrated good psychometric properties, includ-
tional eighth scale, sympathetic magic, which ing good internal consistency for both the disgust
measures respondents’ attitudes about objects propensity (α = 0.89) and disgust sensitivity
that resemble or have had brief contact with dis- (α = 0.87) subscales. The measure has also dem-
gust elicitors from the seven domains. Each sub- onstrated good convergent validity (Davey &
scale of the DS is composed of four items. The Bond, 2006). The DPSS was revised to include
first two items are answered true or false (scored only 16 items (DPSS-R) and has also demon-
0 or 1), and the last two items are assessed on a strated adequate reliability (disgust propensity,
three-point Likert scale ranging from 0 (“not dis- α = 0.78; disgust sensitivity, α = 0.77 (van
gusting at all”) to 1 (“very disgusting”). Three of Overveld et al., 2006)) and good convergent and
the true/false items are reverse-scored (i.e., items discriminant validity (Olatunji et al., 2007a).
1, 4, and 10). The alpha coefficient for the DS is Some research on the role of disgust sensitiv-
0.84, and the alpha coefficient for the eight sub- ity in psychopathology among children and ado-
scales range from 0.34 to 0.60: food, α = 0.34; lescents has relied on the DSQ and DS. For
sympathetic magic, α = 0.44; hygiene, α = 0.46; example, Muris et al. (2008b) measured disgust
body products, α = 0.55; animals, α = 0.47; body sensitivity with both the DSQ and the DS; some
envelope violations, α = 0.60; sex, α = 0.51; modifications to the DS were made before admin-
death, α = 0.59 (Haidt et al., 1994). The reliabili- istering the scale to children. These authors
ties of the individual subscales are quite low; reported that they simplified some items and
thus, scores on individual subscales should be replaced “too offensive formulations” (e.g., “You
interpreted with caution. This scale has not yet see a man with his intestines exposed after an
been adopted for use with children. accident” was changed into “You see a man with
The DSQ and DS are limited to measuring an injured face after an accident”) (p. 136). Muris
disgust propensity (how readily or easily an indi- and colleagues also removed the sex domain
vidual responds with disgust); however, research from the scale because they deemed that these
has demonstrated that disgust sensitivity (the items were inappropriate for children. Lastly,
emotional impact of experiencing disgust) may they changed the response scale for the last 16
contribute to psychopathology. The Disgust items into a Likert scale with four, rather than
three, options: “not at all disgusting,” “somewhat psychophysiological measures (Stark et al.,
disgusting,” “disgusting,” and “very disgusting.” 2005), and behavioral tasks (Klieger & Siejak,
More recently, a version of the DES was 1997; Tsao & McKay, 2004). These alternative
adapted for children, the Disgust Emotion Scale means of measuring disgust sensitivity have not
for Children (DES-C). The DES-C measures dis- only added to the expanding literature on disgust
gust toward the same five factors as the DES: (1) sensitivity but also served as a means of validat-
rotting foods, (2) injection and blood, (3) odors, ing self-report measures. Rozin et al. (1999)
(4) mutilation and death, and (5) animals. The demonstrated that scores on the DS predicted
DES-C consists of 30 items rated on a 0 (no dis- behavior on a series of behavioral tasks designed
gust at all) to 4 (extreme disgust) scale. The to evaluate disgust in a large sample of under-
DES-C has shown good reliability (total scale, graduate students. Rozin et al. found that perfor-
α = 0.93; food subscale, α = 0.91; injection and mance on the behavioral tasks correlated with the
blood subscale, α = 0.88; odors, α = 0.85; mutila- score on the DS for participants who took the DS
tion and death, α = 0.85; animals, α = 0.77), 2 months prior to the behavioral tasks, as well as
excellent convergent validity, fairly good predic- for participants who took the DS immediately
tive validity, and acceptable parent-child agree- following the experiment.
ment. Importantly, the DES-C proved to perform In a sample of children, Muris et al. (2008b)
better on some psychometric indicators than an included a behavioral measure of disgust sensi-
age-downward version of the DS (Muris et al., tivity in addition to the DSQ and DS by asking
2012). the children to select “defiled candy” (p. 135) as
Finally, Viar-Paxton et al. (2015) developed a reward for their participation in the task.
the Child Disgust Scale (CDS), a self-report mea- Children were asked to choose whether they
sure of disgust specific to children. The CDS has would like either “five pieces of fresh chocolate,
18 items that assess sensitivity to core disgust ten pieces of chocolate that had passed the best-
(i.e., items related to oral corporation of contami- before date, or 15 pieces that had been dropped
nants or contact with bodily waste or small ani- on the floor” (p. 137). The authors conducted a
mals), contamination disgust (i.e., items related pilot investigation of their behavioral task with a
to possible contamination by contagion of ill per- sample of 114 children and asked them to rate
sons), and animal-reminder disgust (i.e., items their level of disgust for each of the three condi-
related to threat to the body envelope, injury to tions from 1 (“not at all disgusting”) to 5 (“very
the body, or death). Items are rated on a three- disgusting”) and found that ratings for condition
point response scale (0 = always, 1 = sometimes, 1 were low (M = 1.34, SD = 0.74), but ratings for
2 = never), which was determined to be more conditions 2 and 3 were each significantly higher
developmentally appropriate for children com- (M = 3.68, SD = 1.16 and M = 3.48, SD = 1.21,
pared to a five-point response scale. Research has respectively).
shown that the CDS measures disgust affect and
disgust avoidance, as well as general disgust sen-
sitivity response. The CDS has shown good inter- he Role of Disgust in Psychological
T
nal consistency (α = 0.77) and convergent and Disorders
discriminant validity, suggesting that the CDS is
a developmentally appropriate measure with Although disgust was referred to as the “forgot-
good psychometric properties (Viar-Paxton et al., ten emotion of psychiatry” a decade ago (Phillips
2015). et al., 1998), it has recently emerged as an
Beyond using the typical paper-and-pencil increasingly important variable in psychological
approach to measure disgust sensitivity, other research (Olatunji & McKay, 2007, 2009).
methods have been used including observation of Foremost, trait disgust has been proposed as a
facial expressions (Ekman & Friesen, 1986), central variable in the etiology and maintenance
neuroimaging techniques (Schienle et al., 2005), of some anxiety disorders, including
contamination-related OCD, animal phobias, and exhibited by small animal, BII, and contamination-
BII phobia, all of which are discussed in detail fearful individuals (e.g., Huijding and de Jong
below. Anxiety disorders have primarily been (2007), Sawchuk et al. (1999), Teachman et al.
conceptualized as being phenomenologically and (2001), Tolin et al. (2004)).
etiologically related emotional responses associ- These data suggest that disgust may function
ated with overdeveloped and overgeneralized as a maintenance factor in contamination-related
danger perceptions that result in anxious arousal OCD, animal phobias, and BII phobia (Muris,
(Barlow, 2002; Barlow et al., 2004; Cisler et al., 2006). Although speculative, the pattern of find-
2009). However, the literature investigating the ings described above suggests several avenues by
relationship between disgust and anxiety disor- which this may occur. In accordance with
ders is quickly mounting, and the results have Mowrer’s two-factor model (Mowrer, 1960),
begun to provide a more comprehensive perspec- disgust-related avoidance is likely to minimize
tive on factors involved in avoidance. Indeed, dis- exposure to the avoided stimuli and, conse-
gust sensitivity has been conceptualized as a quently, deprive an individual of the opportunity
dispositional trait that increases the likelihood of to incorporate corrective information into his or
an individual developing avoidance reactions her maladaptive disgust- or fear-related schemata
(McNally, 2002). (Muris, 2006). Thus, a child who actively avoids
In a review of 41 studies examining the emo- spiders would, theoretically, minimize his or her
tional responding toward disorder-relevant stim- opportunities to learn, for example, that he or she
uli, Cisler et al. (2009) demonstrated that spider will not be overwhelmed with disgust or panic
phobia, BII phobia, and contamination-related when a spider is encountered. Second, as avoid-
OCD are all characterized by fear and disgust. ance functions to minimize aversive emotional
The authors of this study investigated fear and states (Barlow, 2002; Barlow et al., 2004), this
disgust across four separate response domains method of coping is likely to be negatively rein-
believed to differentiate between these emotions: forced (Mowrer, 1960). Third, the cognitive
heart rate, cognitive appraisals, facial expression, biases associated with disgust (e.g., sympathetic
and neural substrates. Several additional lines of magic, primary and secondary disgust-related
research have examined disgust’s relationship appraisals, and attentional, perceptual, and mem-
with small animal phobia, BII phobia, and ory biases) may promote the persistence of these
contamination-related OCD and, taken together, dysfunctional schemata and indirectly promote
suggest that disgust may be implicated in the the utilization of avoidance.
pathogenesis and maintenance of these condi- In contrast to the disgust state, the propensity
tions (Olantunji et al., 2010). First, self-report to experience disgust (i.e., trait disgust) appears
measures of disgust propensity have repeatedly to be a specific, genetically based vulnerability
been associated with self-report measures of factor to the development of contamination-
these conditions (e.g., Olantanji and Cisler related OCD, animal phobias, and BII phobia
(2009)). Second, research has demonstrated that (Muris, 2006). More specifically, on the basis of
persons with elevated spider fears, BII phobia, the results of mediational studies, Olatunji et al.
and contamination fears report feelings of disgust (2010) suggest that disgust propensity may medi-
when exposed to associated stimuli (e.g., Deacon ate the relationship between general vulnerabili-
and Olatunji (2007), Sawchuk et al. (2002), Tolin ties (e.g., negative affectivity,
et al. (1997)). Third, self-reported disgust is contamination-related cognitions, contamination
related to avoidance of spiders, BII-related stim- fear) and the aforementioned anxiety disorders.
uli, and contamination-related stimuli (e.g., In other words, mediational studies suggest that
Deacon and Olatunji (2007), Olatunji et al. these higher-order factors contribute to the devel-
(2008a), Tsao and McKay (2004), Woody et al. opment of spider phobia, BII phobia, and
(2005)). Fourth, studies have indicated that dis- contamination-related OCD via one’s proclivity
gust plays a critical role in the cognitive biases to experience disgust. According to the authors
(Olantunji et al., 2010), (a) disgust propensity 139]) to Dutch school children about unknown
may play a role in these conditions via interpreta- Australian marsupials. The results indicated that
tion biases, attentional biases, or dread of conta- disgust-related information induced both higher
gion, (b) anxiety sensitivity and difficulties in levels of disgust and fear in relation to these ani-
general emotional regulation may potentiate the mals, while the cleanliness-related information
relationship between disgust propensity and con- decreased disgust and fear toward the animal.
tamination and spider fears, and (c) parental dis- Another study by Muris et al. (2012) presented
gust propensity may be implicated in the children with either disgust-eliciting specimens
development of spider phobia and, pending fur- of the cuscus (e.g., excrements) or neutral speci-
ther research, BII phobia and contamination- mens of the cuscus (e.g., piece of clean, well-
related OCD. combed fur). Children in the disgust specimen
group exhibited an increase in fear toward the
cuscus and a stronger inclination to interpret
Animal Phobias ambiguous situations involving the cuscus in a
more negative way compared to children in the
Although there is ample evidence from research neutral specimen group. These two studies pro-
with adults for a disgust conceptualization of ani- vide compelling evidence that disgust-related
mal phobias (e.g., Matchett and Davey’s (1991) information increases fear of unknown animals.
disease-avoidance model), there have been far With regard to disgust sensitivity and small
fewer studies with pediatric samples. In a sample animal phobias, research has primarily focused
of school children aged 8–13 years in the on spider phobia in particular (de Jong et al.,
Netherlands, Muris et al. (1999) found that dis- 1997; de Jong & Muris, 2002). With a sample of
gust sensitivity as measured by the DSQ was sig- 22 spider-phobic girls, de Jong et al. (1997) found
nificantly correlated with animal phobias, even that not only was disgust sensitivity significantly
when controlling for trait anxiety (r = 0.14). correlated with fear of spiders but also ratings of
Muris et al. (2008b) also found that DS and DSQ disgust decreased along with fear after successful
scores were both significantly correlated with treatment. Specifically, the authors found that
small animal phobias (mean r = 0.42) and spider spider-phobic girls had had higher disgust sensi-
phobia (mean r = 0.36) for boys and girls aged tivity and found spiders in particular more dis-
9–13 years. Furthermore, these researchers found gusting than did nonphobic controls. Additionally,
that the DS animals subscale in particular was they found that disgust associated specifically
specifically related to small animal and spider with spiders was reduced through treatment using
phobia. In a behavioral test, in which children eye movement desensitization and reprocessing
were asked to select from clean or contaminated (EMDR) as well as in vivo exposure. However,
candy as a reward, the results were significantly the level of disgust sensitivity, as measured by the
correlated with small animal and spider phobia DSQ (Rozin et al., 1984), remained unaffected
for girls only. by treatment targeting the spider phobia.
Muris et al. (2008a) demonstrated that fear to In a follow-up study, de Jong and Muris (2002)
an unknown animal can be experimentally compared a sample of 18 spider-phobic girls to a
induced in children by providing disgust-related group of 18 nonphobic girls on their ratings of
information about the animal. In this study, Muris disgust sensitivity as well as their ratings of the
and colleagues provided disgust-related informa- subjective likelihood of a spider to enter their pri-
tion (e.g., “When a cuscus/quokka has to urinate vate living space, spiders’ tendency to approach
or to relive himself, he just does it in the hole and make physical contact, and the subjective
where he also sleeps” [p. 139]) and cleanliness- probability of spiders doing physical harm. The
related information (e.g., “The cuscus/quokka results indicated that spider-phobic girls reported
lives in a hole which smells nice. This is because significantly higher levels of disgust sensitivity
he decorates his bed with petals and flowers” [p. and found spiders more disgusting than
nonphobic girls. Notably, phobic girls in this most strongly associated with washing and
study reported higher ratings concerning spiders’ checking symptoms in OCD. Muris et al. (2000)
tendency to enter their living space and approach found that obsessive-compulsive symptoms,
and make contact with them. The authors hypoth- especially cleaning concerns, were significantly
esize that the combination of increased disgust related to disgust. Olatunji et al. (2005) also
sensitivity and cognitions related to increased found that disgust sensitivity was a predictor of
likelihood of making physical contact leads to the high levels of contamination fear.
development of spider phobia. It is interesting to Moretz and McKay (2008) investigated the
note that the results indicated that the critical relationship between OCD contamination symp-
variable in distinguishing between the phobic toms, trait anxiety, and disgust sensitivity in a
and nonphobic girls in regression analyses was large sample of undergraduate students (N = 740).
the perceived ability of spiders to contaminate a Using structural equation modeling, disgust sen-
chocolate bar (i.e., response to the items: “How sitivity, as measured by the DS, was directly and
much would you like to eat your favourite choco- positively associated with contamination fear and
late bar after a spider has walked across the bar washing rituals. The relationship between disgust
when it is still wrapped in its package?” and sensitivity and contamination and washing OCD
“How much would you like to eat your favourite symptoms was neither fully nor partially medi-
chocolate bar after a spider has walked across the ated by trait anxiety, which indicates that
unpacked bar?” [de Jong et al., 1997, p. 560]). contamination- based OCD symptoms may be
Cognitions regarding the likelihood for a spider better conceptualized as resulting from increased
to approach and make contact had no additional disgust rather than fear.
predictive value in this study, which is a strong To date, there has been very little research to
evidence that spider phobia is most closely date on the connection between OCD and disgust
related to disgust sensitivity. sensitivity in pediatric samples. In a sample of
school children aged 8–13 years in the
Netherlands, Muris et al. (1999) found that dis-
Obsessive-Compulsive Disorder gust sensitivity as measured by the DSQ was sig-
nificantly correlated with OCD symptoms
In addition to phobias, a growing body of research (r = 0.30), but this correlation lost significance
has indicated that there is a relationship between when trait anxiety was held constant. In another
disgust sensitivity and OCD. Fear of contamina- nonclinical sample, Muris et al. (2008b) found
tion has been identified as one of the most com- that DS and DSQ scores were both significantly
mon obsessive concerns among people who correlated with OCD symptoms for boys aged
suffer with OCD (Foa & Kozak, 1995; Foa et al., 9–13 years. For girls in the sample, DS score was
1995), and this preoccupation with avoiding con- significantly correlated with OCD symptoms, but
tamination points to a plausible relationship the DSQ score was not significantly correlated.
between disgust sensitivity and OCD. Tolin et al. Furthermore, these researchers found that the DS
(2006) suggested that disgust may uniquely con- hygiene subscale in particular was specifically
tribute to contamination-based OCD because related to OCD symptoms. In a behavioral test of
feelings of disgust lead to phobic avoidance of disgust sensitivity, there was a significant corre-
certain stimuli that are relieved through compul- lation between disgust sensitivity and OCD
sive behavior and the behavior is sustained symptoms for boys only. More recently, a study
through negative reinforcement. of the degree to which fear, incompleteness, and
There is ample empirical research linking dis- disgust are associated with the main symptom
gust sensitivity and OCD symptoms in adult sam- dimensions of OCD (aggressive, symmetry, con-
ples (Mancini et al., 2001; Schienle et al., 2003b; tamination) conducted with a sample of youth
Thorpe et al., 2003). In particular, research has with OCD found that while disgust was involved
suggested that disgust sensitivity appears to be in all three OCD symptom dimensions, it was
most strongly linked to contamination symptoms latter phase of the diphasic response is hypothe-
(Cervin et al., 2020). Finally, Knowles et al. sized to be state disgust (Page, 1994, 2003; Page
(2016) investigated the relationship between & Tan, 2009).
changes in disgust proneness and disorder- While the incidence of fainting among BII
specific symptoms during residential treatment phobic children has not been reported, a signifi-
among youth aged 12–18 with OCD, anxiety, and cant minority of adolescents faint in response to
mood disorders. They found that reductions in BII stimuli (Kleinknecht & Lenz, 1989), and
disgust were greatest among youth with primary fainting in response to presentation of a “nox-
OCD and that OCD symptoms, compared to ious” or “emotional” stimulus has been docu-
other symptoms, were most strongly correlated mented in children and adolescents (Driscoll
with reductions in disgust proneness. These pre- et al., 1997). These findings, in conjunction with
liminary results are similar to findings in adult the early age of onset of BII phobia (Bienvenu &
populations and indicate a link between disgust Eaten, 1998; Marks, 1988; Ost, 1992), current
and OCD, but there is a clear need for more etiological theories of BII phobia (Olatunji et al.,
research utilizing clinical pediatric samples. 2008a, 2006b; Page, 1994; Page & Tan, 2009),
and modern adaptationist conceptualizations of
fainting in response to BII-related stimuli
Blood-Injection-Injury Phobia (Bracha, 2004), suggest that fainting may directly
influence the etiology and maintenance of the
Discomfort upon exposure to blood, injury, and disorder in children.
needles is a common phenomenon in childhood Trait disgust has also been moderately to
and adolescence. Research indicates that between strongly correlated with BII fear, BII fainting,
one-quarter and one-half of children experience and BII avoidance (e.g., de Jong and Merckelbach
mild BII fears (Lapouse & Monk, 1959; Marks, (1998), Muris et al. (1999, 2008b), Olatunji et al.
1988). For approximately 3% of children and (2008, 2006a, b), Page (2003), Schienle et al.
adolescents, however, BII fears are severe and (2001)). For example, Muris and colleagues
debilitating enough to warrant a clinical diagno- (1999) examined the relationship between trait
sis (Marks, 1988; Miller et al., 1974). Research disgust and BII phobia symptoms in nonclinical
has revealed that BII phobia is closely related to children and found that trait disgust was moder-
disgust (de Jong & Merckelbach, 1998; Olatunji ately correlated with BII phobia symptoms, even
et al., 2005; Page, 1994, 2003; Sawchuk et al., after controlling for levels of trait anxiety. In a
2002; Tolin et al., 1997). more recent study, Muris et al. (2008b) found sig-
Disgust reactions (i.e., state disgust) are nificant positive correlations between trait dis-
believed to be centrally involved in BII phobia- gust and symptoms of BII phobia, which were
related fainting (Page, 1994, 2003; Page & Tan, not attenuated when controlling for neuroticism
2009). Upon presentation of BII stimuli, individ- (i.e., the tendency to experience negative affect).
uals exhibit a biphasic response characterized by Finally, disgust-related cognitive processes
an initial surge in sympathetic nervous system are also speculated to be involved in the patho-
activity, rapidly followed by a drop in blood pres- genesis and maintenance of BII phobia (Olantunji
sure and heart rate. If the drop in blood pressure et al., 2010; Page & Tan, 2009). As described
is precipitous enough to impede cerebral blood above, the cognitive processing of disgust-related
flow, fainting and, to a lesser extent, seizures can information is often biased by the laws of conta-
occur (Bienvenu & Eaten, 1998; Graham et al., gion and similarity (i.e., law of sympathetic
1961; Marks, 1988; Page, 1994, 2003). Fear is magic; Rozin & Fallon, 1987; Teachman, 2006),
likely responsible for the initial increase of sym- pathological disgust reactions are characterized
pathetic nervous system activity (Olatunji et al., by disgust-related primary and secondary
2008b; Page, 1994, 2003; Thyer & Curtis, 1985); appraisals (Teachman, 2006), and disgust may be
the mechanism responsible for the shift into the associated with unique attentional, perceptual,
and memory biases (Williams et al., 2009). this kind of unambiguous direct connection
Unfortunately, only limited research has investi- between parental modeling and learning. For
gated the relationships between these cognitive example, recent evidence suggests that many
phenomena and BII phobia. Future research phobias arise without any direct experience with
should attempt to continue to elucidate these the phobic stimulus and that in some instances,
associations and to further determine the extent conditions that learning theory would predict the
to which these constructs are involved in child- onset of phobias instead show substantial
hood BII phobia specifically. approach behavior for the same stimulus (detailed
in Menzies and Clarke (1995)).
While the parental modeling approach appears
Preliminary Model of Disgust
A to effectively instruct children on disgust for food
in Childhood Anxiety Disorders and objects resembling disgust-related stimuli,
this only accounts for one facet of disgust. Recent
The available evidence suggests that disgust research has suggested that the seven disgust
plays a role in several different anxiety problems elicitors comprise three larger categories, namely,
that manifest in childhood. In light of the research core (which includes food and body products),
conducted illustrating a connection between animal reminder (such as body envelope viola-
avoidance and disgust and the basic research on tions and sex), and contamination (prominently
the development of disgust-related aversions, a featuring sympathetic magic). These domains,
preliminary model may be considered to guide identified in psychometric evaluations of the dis-
future research. gust scale (Olatunji et al., 2007c), have unique
behavioral, psychophysiological, and self-report
correlates when examined with undergraduate
Development of Disgust and community samples (Olatunji et al., 2008b).
How these disparate forms of disgust develop is
As discussed earlier, infants show the capacity to not clear, although each has been found in multi-
express disgust reactions. However, perhaps cultural evaluations (Olatunji et al., 2009).
more than other emotional states, disgust for spe- Sawchuk (2009) suggests that older children
cific objects is taught by caregivers and other and adolescents develop more sophisticated
environmental sources (Sawchuk, 2009). The appraisal processing skills that, in conjunction
most basic learning for disgust involves adverse with normal neural development, allows for
reactions to food-related stimuli that would be greater distinctions among potentially disgust-
deemed unpalatable, either due to risks of ingest- evoking stimuli and situations that would pose
ing toxins for similar appearing foods (e.g., eat- risks for contamination and other harms.
ing candy shaped like feces) or for culturally Accordingly, sympathetic magic and its associ-
specific reasons (e.g., proscribing consumption ated laws of similarity and contagion have their
of uncooked vegetables in some Chinese cul- roots in parental instruction but gain greater
tures). The underlying basis for how disgust is prominence in more elaborate situational
acquired has recently focused on evaluative con- appraisal that comes with cognitive
ditioning, as discussed earlier (de Houwer et al., development.
2001). To summarize, the act of labeling an
object, in conjunction with the modeled reactions
of caregivers, produces a powerful learning expe- Internal Evaluation and Appraisal
rience that consolidates the emotional reaction
and leaves it resistant to extinction. As children develop greater appraisal processing
It is interesting to note that disgust is unique in skills, anxiety can be conferred by increased
this regard. Other emotional states associated internal monitoring. Anxiety sensitivity has been
with psychopathological conditions do not show shown to be a potent explanatory construct for a
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Problems in Emotion Regulation
in Child and Adolescent Anxiety 13
Disorders Section: Diagnostic
Components of Child
and Adolescent Anxiety Disorders
Kristel Thomassin, Marni L. Jacob, Kara B. West,

Molly E. Hale, and Cynthia Suveg
heoretical Foundations of Emotion

T service of one’s goals (Thompson, 1994). ER
Regulation in Anxiety Disorders involves an awareness of an emotional experi-
ence, the ability to appraise the context surround-
In the first edition of this chapter, over a decade ing the emotional experience, and modification
ago, we noted that the field of psychology was in of emotional expression given social context
the midst of an emotion revolution, with much of demands. ER is part of a larger dynamic, biobe-
that work specifically focused on the construct of havioral system of self-regulation in which cog-
emotion regulation (ER). Indeed, our understand- nitive, behavioral, and physiological components
ing of the ways that ER is involved in youth psy- are reciprocally related to one another and are
chopathology broadly, and anxiety specifically, has influenced by environmental experiences (Blair
increased dramatically as a result of this work and et al., 2011; Fox & Calkins, 2003).
has recently been summarized in narrative reviews ER underlies healthy functioning across the
and meta-analyses (e.g., Mathews et al. (2016), life span, and difficulties in this developmental
Sendzik et al. (2017), Schäfer et al. (2017)). process have been linked to various forms of psy-
Despite the plethora of works examining ER chopathology. In this way, ER is a transdiagnos-
in child psychopathology in the past decade (and tic process that underlies various forms of
prior), debates still exist regarding the conceptu- psychopathology, both internalizing and exter-
alization and operationalization of ER. In this nalizing (Aldao et al., 2016). Although difficul-
chapter, we define ER as a set of processes ties in ER are not specific to anxiety disorders,
required for the modification of emotional expe- there are certain patterns of emotional arousal
riences based on contextual demands and in the and ineffective emotion management that are
associated with childhood anxiety disorders in
particular and that are influenced by contextual
K. Thomassin (*)
variables such as parenting (Allen et al., 2016;
University of Guelph, Guelph, ON, Canada
e-mail: Kristel.Thomassin@uoguelph.ca Mathews et al., 2016; Schäfer et al., 2017; Tan
et al., 2020; Whitehead & Suveg, 2016). Clinical
M. L. Jacob
Jacob Center for Evidence-Based Treatment, scientists have attempted to translate these basic
Boca Raton, FL, USA research findings into empirically supported
K. B. West · M. E. Hale · C. Suveg interventions for child anxiety with mixed results
University of Georgia, Athens, GA, USA (Kennedy et al., 2019; Suveg et al., 2018). In this
https://doi.org/10.1007/978-3-031-14080-8_13
192 K. Thomassin et al.
chapter, we illustratively, though not exhaus- tem). In addition to alterations in neural connec-
tively, review this literature. We conclude with a tivity and activation, youth with anxiety show
critical synthesis of the work and offer sugges- neurostructural abnormalities in brain regions
tions for future research in this area. involved in emotion regulation such as decreased
gray matter volume in the amygdala, ventrome-
dial prefrontal cortex, and hippocampus (for a
iological Foundations of Emotion
B review, see Strawn, Lu, Peris, Levine, & Walkup,
Regulation in Anxiety 2021).
Research has also identified physiological
Neurobiological and genetic factors are pivotal in processes implicated in both emotion regulation
considering the development of ER because their and anxiety. For example, vagal tone, a measure
influence is present from birth. Although there is of the balance between the sympathetic and para-
no single genetic marker for anxiety disorders, sympathetic nervous systems, is considered a
there are structural and functional abnormalities psychophysiological marker that underlies criti-
in neurobiological systems and patterns of reac- cal self-regulatory processes (see Holzman and
tivity that are associated with anxiety (e.g., for a Bridgett (2017) for a review). Low vagal tone is
review, see Strawn et al., 2021). Specifically, sev- typically associated with ER deficits and difficul-
eral major neurobiological systems are associ- ties managing emotionally arousing situations
ated with the elicitation, experience, and (Beauchaine & Bell, 2020). In contrast, high
regulation of emotions (e.g., amygdala, prefron- vagal tone has also emerged as a potential protec-
tal cortex, vagal tone), and a growing body of lit- tive factor in the link between risk factors (e.g.,
erature has linked anxiety with abnormalities in behavioral inhibition, cognitive biases) and anxi-
such substrates (Blackford & Pine, 2012; Strawn ety symptoms in children (Trent et al., 2020;
et al., 2014). Viana et al., 2017). Nonetheless, neurobiological
The amygdala in particular plays an essential and physiological factors alone are not sufficient
role in emotion management and arousal (Fox to explain why some youth develop anxiety dis-
et al., 2015; Janak & Tye, 2015), and children orders and others do not. It is the interplay of
with anxiety disorders have been shown to exhibit these factors with other temperamental, cogni-
greater amygdala responses to fearful stimuli tive, and environmental influences that accounts
than nonanxious children (Williams et al., 2015). for a child’s vulnerability to developing an anxi-
Frontal cortical regions of the brain that are ety disorder (Davis et al., 2017; Degnan et al.,
involved in modulating amygdala activity are 2010).
also highly involved in ER activity (Janak & Tye, Behavioral inhibition (BI), a temperament
2015). For instance, youth with higher levels of style characterized by fear, shyness, and avoid-
anxiety and behavioral inhibition (a temperamen- ance of novel situations and people (Fox et al.,
tal style discussed below) show increased pre- 2005), has been identified as a robust risk factor
frontal activation (Fu et al., 2017). Animal and for the development of anxiety disorders in youth
human studies suggest that there may be a dis- (Sandstrom et al., 2020). Temperament is closely
tinct fear circuitry system in the brain connecting tied with children’s emotion regulation abilities
the amygdala and prefrontal cortex that serves as (Rothbart & Bates, 2006); behaviorally inhibited
a neural basis for anxiety disorders (Duvarci & children tend to engage in avoidance and with-
Pare, 2014; Fox et al., 2015). In brief, this fear drawal to manage anxiety, which in turn main-
circuitry system involves key brain regions (e.g., tains their heightened reactivity to fear and limits
amygdala, hippocampus, prefrontal cortex) that their opportunities to learn better emotion regula-
are implicated in threat perception, fear learning, tion strategies (Stifter et al., 2011). Importantly,
and the experience and modulation of the fear not all children initially classified as inhibited
response (see Duvarci and Pare (2014) for a more remain inhibited across time (Tang et al., 2017),
thorough explanation of this fear circuitry sys- and a variety of intrinsic (e.g., neurobiological)
13 Problems in Emotion Regulation in Child and Adolescent Anxiety Disorders Section: Diagnostic… 193
and extrinsic (e.g., parental, familial, life stress) physiology, thus highlighting the value of multi-
factors likely contribute to the variability in method data.
outcomes (Lahat et al., 2011; Ryan & Ollendick, Youth with anxiety also show deficits in the
2018). Research suggests that children display- cognitive strategies used to regulate emotional
ing extreme levels of inhibition likely maintain experiences in response to stressful negative
their classification years later and are at the great- events (i.e., cognitive ER). Cognitive strategies
est risk of subsequent anxiety disorder develop- such as catastrophizing and rumination are con-
ment (Chronis-Tuscano et al., 2009; Vreeke sidered maladaptive whereas positive reappraisal
et al., 2013). Previous research suggests that and refocusing are adaptive (Garnefski et al.,
early temperamental risk could be moderated by 2007). Several studies have found that anxious
parenting factors over time. As one example, youth use maladaptive cognitive ER more and
overinvolved parenting may reduce opportunities adaptive cognitive ER strategies less than their
for youth to experience novel, difficult situations nonanxious peers (Chan et al., 2016; Garnefski
and thus preclude them from developing a reper- et al., 2002). For instance, in a sample of
toire of effective ER strategies and the self- 9–11-year-old youth, those with anxiety disor-
efficacy needed to enact them (Ollendick & ders endorsed catastrophizing and rumination
Grills, 2016). more and positive reappraisal and refocus less
than did youth without disorders (Legerstee et al.,
2010). Relatedly, another study by Suveg et al.
ognitive Foundations of Emotion
C (2010) found that youth with anxiety disorders
Regulation in Anxiety engage in fewer problem-solving strategies over-
all when managing their emotions than nonanx-
Emotion regulation and cognitive processes are ious youth.
closely intertwined, and these domains can inter- In part, the ER difficulties that anxious youth
act in ways that influence anxiety development experience may be related to their low sense of
and maintenance (Trent et al., 2020). For instance, self-efficacy in managing negative events. Several
the tendency to interpret ambiguous situations in studies have found that anxious children have
a threatening manner is associated with anxiety lower self-efficacy than nonanxious youth
in youth both concurrently and prospectively (Muris, 2002; Muris et al., 2009; Suveg & Zeman,
(Cannon & Weems, 2010; Dodd et al., 2012). 2004). Lower self-efficacy results in increased
Increases in negative emotion as a result of doubts regarding the ability to control emotional
threatening interpretations may become increas- experiences and responses in arousing situations
ingly difficult to manage and pose threats to (Suveg & Zeman, 2004). Collectively, low self-
effective ER. On the flip side, youth with ER dif- efficacy in combination with poorer ER likely
ficulties may have difficulties generating and leads youth with anxiety disorders to avoid or
using cognitive strategies to effectively regulate give up in emotionally challenging situations,
emotional experiences. Recently, in a sample of which further reinforces their cognitions regard-
8–12-year-old children with anxiety disorders, ing their abilities to handle future emotionally
Trent et al. (2020) found that child interpretation challenging situations. Although avoidance is
biases were associated with more severe anxiety effective in the short term by producing immedi-
symptoms but only in the context of poor vagal ate reductions in anxiety, it prevents the child
regulation (conceptualized as a physiological from learning to regulate emotional arousal and
index of ER), suggesting a buffering effect of achieve a sense of mastery over the anxiety-
high vagal regulation. Further, the combination provoking event. Counterproductively, this
of poor vagal regulation and interpretation biases avoidance will serve to maintain a child’s fears
was associated with the most severe anxiety and may hinder him/her broadly, primarily
symptoms. This study documents the complex through restricting social, academic, and other
interplay of ER, cognitive processes, and even opportunities.
Environmental Foundations able and potentially dangerous (Becker &

of Emotion Regulation in Anxiety Ginsburg, 2011).
Peers also have a substantial impact on a
Environmental influences have been strongly child’s ER and anxiety. Particularly as youth
implicated in the link between children’s ER and enter into adolescence, they spend more time
anxiety. While there are a wide range of environ- with their peers than anyone else (Lerner &
mental influences (e.g., children’s opportunity to Steinberg, 2009). With increased autonomy and
observe and practice ER skills, children’s expo- decreased parental supervision, friendships
sure to emotionally charged scenarios, parent and become more intimate and places of greater emo-
peer responses to children’s emotional displays, tional support (Voile, 2010). When adolescents
sociodemographic and cultural factors (Schäfer receive supportive socialization from their friends
et al., 2017)), this chapter focuses on two that (e.g., validation, distraction) when experiencing
have received much support – parents and peers intense emotional arousal, they are more likely to
(Miller-Slough & Dunsmore, 2019). seek support again (Legerski et al., 2015), poten-
One of the most prevalent ways parents and tially buffering against the development of psy-
peers influence a youth’s ER and anxiety is chopathology (Rubin et al., 2008). However,
through a process called emotion socialization poor quality friendships or a lack of friendships
(for review, see Miller-Slough and Dunsmore may confer risk for the development of anxiety
(2016)). Emotion socialization is the mechanism disorders. Adolescents who experience emotion
through which others teach children appropriate neglect from their peers may begin to feel iso-
ways to express and regulate their emotions lated, decreasing the likelihood that they will
(Eisenberg et al., 1998). Parents are thought to be continue to seek emotional support. This gives
the first socializers of their children’s emotions, way to increased emotional suppression as well
monitoring youth’s exposure to emotional expe- as risk for anxiety (Legerski et al., 2015). Further
riences and acting as filters of children’s emo- work has noted that adolescents who experienced
tional environments (Denham et al., 2015). more punitive socialization of their emotions by
Parents who are less accepting of a child’s emo- peers reported increases in somatic complaints
tional displays may reinforce a youth’s inhibition over time, a common symptom of anxiety disor-
of emotion, thus leading to fewer opportunities to ders (Parr et al., 2016). Taken together, it is likely
learn successful coping strategies and therefore that several parental, peer, and child factors inter-
increase the risk of developing anxiety (Sarıtaş act to result in emotion dysregulation in youth
et al., 2013). In contrast, parents who engage in with anxiety disorders.
more supportive forms of socialization (e.g., vali- When examining emotion regulation and
dation of a child’s emotions, calm and pleasant anxiety disorders in youth, gender differences
affect when engaging with the child) may buffer have been noted across emotion competencies.
against a child’s anxious affect (Oppenheimer For example, a meta-analysis by Chaplin and
et al., 2016). Parents of anxious children may Aldao (2013) demonstrated that middle child-
also show low levels of emotional expression and hood girls expressed significantly more positive
flexibility as well as engage in maladaptive emotions and internalizing emotions (i.e., sad-
socialization techniques (e.g., high levels of neg- ness and anxiety) whereas boys expressed sig-
ativity and intrusiveness) during emotional expe- nificantly more externalizing emotions (i.e.,
riences with their child (Hudson et al., 2008; Van anger). In terms of anxiety, Bender et al. (2012)
der Giessen & Bögels, 2018). Further, parents of found emotion dysregulation to be more predic-
anxious children are more likely to be suffering tive of anxiety in girls relative to boys. Finally,
from anxiety themselves and might model anx- Stone and colleagues (2019) found that co-dis-
ious or avoidant behaviors when faced with an traction (vs. distraction alone) was effective at
anxiety-provoking situation. This, in turn, may regulation of negative affect in anxious girls, but
signal to children that the event is insurmount- not in boys. Gender differences are also noted in
peer relationships. For example, girls are more ssessment of Emotion Regulation
A
likely to expect supportive socialization from in Childhood Anxiety
their friends and less likely to anticipate unsup-
portive socialization when compared to boys Experts agree that emotion regulation operates at
(Klimes-Dougan et al., 2014). Girls with anger physiological, behavioral, cognitive, and experi-
dysregulation may be at greater risk for peer ential substrates, and have thus called for inte-
victimization when compared to boys (Morelen grated approaches to measuring child emotion
et al., 2016). regulation. Despite these calls, only 4.5% of pub-
Finally, some studies have suggested that lished studies assess emotion regulation using
socialization and child ER strategies may vary multiple methods (Adrian et al., 2011). Rather
between cultures and other sociodemographic than serving as an exhaustive review, the purpose
variables (Cole et al., 2006). With respect to of the following section is to illustrate various
socialization, for example, Western cultures tend methodological approaches to measure ER in
to be more emotionally expressive and discuss youth including questionnaires, experimental
emotions more freely when compared to Eastern tasks and behavioral observation, ecological
cultures (Morelen et al., 2013). Additionally, cur- momentary assessment, and biological and neu-
rent emotion socialization frameworks, typically roscience methods.
grounded in Western culture, often place a greater
emphasis on youth’s autonomy (Friedlmeier
et al., 2011). Despite this, the notion that ER is a Questionnaires
risk factor for anxiety is a robust finding across
cultures (McLaughlin et al., 2011). Nonetheless, Questionnaire methods range from youth self-
in recent years, a burst of research in this area has report measures to caregiver and teacher reports,
yielded specific findings based on cultural back- and they target the full spectrum of ER and
ground. For example, Varela et al. (2019) found related functions from negative emotionality or
that Latinx youth who endorsed greater anxiety reactivity to the use of specific emotion regula-
exhibited poor emotional awareness. In Chinese tion strategies. When asking youth to report on
samples, research suggests that Chinese adoles- their emotional experiences, it is important to
cents are more likely than children in Western take into account potential developmental con-
cultures to suppress their positive facial expres- straints. For example, youth may not possess the
sions in an attempt to maintain harmony (Deng self-awareness necessary to make such reports,
et al., 2013). And finally, work by Folk et al. particularly when below the age of 5 years
(2014) assessed predictors of anxiety in urban (Kazdin & Weisz, 2003). Obtaining ER data from
minority youth (77.5% Black) and found anger youth themselves, when appropriate, is ideal
and sadness dysregulation as well as worry inhi- given that emotional experiences are not always
bition significantly predicted anxiety 2 years expressed outwardly; thus, only youth may be
later. Taken together, predictors of anxiety and aware of and able to report on their internal emo-
influences on emotion regulation are highly inter- tional experiences.
twined with cultural and sociodemographic Examples of such measures include the
factors. Children’s Emotion Management Scales (CEMS;
See Fig. 13.1 for an illustrative conceptual- Zeman et al., 2001), which assess inhibition as
ization of the various pathways to the develop- well as dysregulation and ER coping. The How I
ment of ER in youth with anxiety disorders. The Feel questionnaire (HIF; Walden et al., 2003)
figure, which was adapted from Suveg, Morelen, measures emotional arousal (i.e., frequency and
Brewer, and Thomassin (2010), is not exhaustive intensity of emotion) and emotion control. The
and highlights only some of the potential vari- Emotion Expression Scale for Children (EESC;
ables involved in ER in youth with anxiety Penza-Clyve & Zeman, 2002) measures emotion
disorders. awareness and willingness to express negative
Cultural
Maladapt ive
Variat ion and
Emot ion
Gender
Socializat ion
Dif ferences
High Child
Temperamental
React ivity
Cognit ive
Biological Environmental Cognit ive Processing
Factors Factors Factors Dif f icult ies
Neurobiological
and Genet ic
Factors
Avoidance,
Child Emot ion Dysregulated
Dysregulat ion Expression,
Inhibit ion
Child Anxiety
Fig. 13.1 Illustrative model depicting several of the major variables involved in child emotion dysregulation and anxi-
ety disorders
emotion. Other questionnaires measure specific measurement. For example, the Child and
aspects of regulation such as the Cognitive Adolescent Dispositions Scale (CADS-P/
Emotion Regulation Questionnaire (CERQ, ages CADS-Y; Lahey et al., 2010) includes a subscale
12 and older (Garnefski et al., 2001)) and the measuring negative emotionality more broadly,
Cognitive Emotion Regulation Questionnaire – and the Regulation of Emotion Systems Survey
kids version (CERQ-k, ages 9–11 (Garnefski (RESS; De France & Hollenstein, 2017) assesses
et al., 2007)), which measure nine cognitive ER specific regulation strategy use (i.e., distraction,
strategies (e.g., self-blame, catastrophizing, posi- rumination, arousal control, reappraisal, engage-
tive reappraisal) that children and adolescents ment, and suppression).
may use after the experience of negative life
events.
Several instruments have been developed for Experimental Tasks and Behavioral
completion by caregivers and teachers. The Observation Methodology
Emotion Regulation Checklist (ERC; Shields &
Cicchetti, 1997), for example, is arguably the A myriad of experimental laboratory tasks have
most commonly used measure assessing caregiv- been used to elicit emotion in youth samples.
er’s perceptions of their child’s ER abilities. These tasks lend themselves to measuring task
Finally, some instruments have parallel youth performance, affective and behavioral displays,
and caregiver report to facilitate multireporter and ER strategy use. The disappointing gift para-
digm (Saarni, 1984), for example, creates posi- some adaptations should be made for children
tive expectations within the child of receiving a younger than 7 years old (Heron et al., 2017). In
desired reward. When this gift violates the addition, when combined with novel statistical
youth’s expectations, children are then expected approaches such as the Network Analysis (e.g.,
to appropriately modulate their emotions and fol- Pe et al. (2015)), EMA researchers can capitalize
low socially acceptable display rules. Coding on the value of temporal emotion dynamics, a
techniques such as microanalytic coding and promising avenue for researchers wanting to
global coding have been suggested for facial study how emotion and ER unfold over time and
expressions, tone of voice, emotions expressed, in “real life.”
and intensity of emotion (e.g., Thomassin and
Suveg (2014)). Other researches have utilized
emotion discussions (e.g., asking a youth to talk Neuroscience Methodology
about times when they felt discrete emotions),
which are then coded for variables such as the Researchers have implicated several biological
strategy that the youth implemented when feeling systems in emotion processing such as the auto-
the emotion and their affect during the discus- nomic nervous system, hypothalamic-pituitary-
sion. Research using this paradigm with both adrenal (HPA) axis, amygdala, and lateral
typical and anxious populations has yielded prefrontal cortex (LPFC). Common methods of
interesting results (e.g., Hudson et al. (2008)). assessment include vagal tone (Beauchaine &
Tasks such as the Trier Social Stress Test have Bell, 2020), cortisol (e.g., Jentsch et al., (2019)),
been widely used and can assess performance and imaging (e.g., fMRI (Dixon et al., 2017)).
(e.g., see the ESPM observational coding scheme Affective neuroscience research in particular has
(Rith-Najarian et al., 2014)) as well as physiolog- blossomed in recent years. In one study, for
ical arousal (Seddon et al., 2020; Thomassin example, the authors found that connectivity
et al., 2018). Finally, experimental tasks, such as between the amygdala and the ventromedial PFC
the cognitive reappraisal task (McLaughlin et al., may be particularly relevant to the development
2015), can instruct youth to apply specific regula- of internalizing disorders in adolescence (Burghy
tion strategies and measure the impact of those et al., 2012). Further, research suggests that dys-
strategies. Given the complexity of this task, it is functional activation patterns during cognitive
typically used with older youth. reappraisal, an ER strategy, can be identified in
individuals with anxiety and mood disorders
(Picó-Pérez et al., 2017). Although significant
cological Momentary Assessment
E advances have been made, this area is still devel-
(EMA) oping quickly, and additional research is war-
ranted, particularly for youth and youth with
Since the last edition of this chapter, the EMA anxiety disorders.
literature has grown considerably, for good rea- Overall, the literature on assessment of ER
son. EMA of emotion and ER has much to offer, requires the continued use of multimethod and
particularly by addressing potential threats to multireporter approaches to help increase our
ecological validity found in laboratory studies. understanding of emotion assessment reliability
Further, EMA fits with the conceptualization of and validity for youth. Further research is needed
emotion and ER as transitory and dynamic con- to develop and validate measures that allow us to
structs. A full review of EMA is beyond the scope accurately capture emotional variability across
of this section, but it should be noted that recent contexts, moment-to-moment changes in ER
meta-analyses have shown that EMA is feasible strategy use, and underlying biological systems
with children as young as 7 years old and that associated with ER.
motion Regulation Considerations

E outcomes. Pretreatment emotion dysregulation
in the Treatment of Childhood did not moderate treatment outcomes. The results
Anxiety were somewhat surprising given preliminary
work showing the superiority of ECBT over CBT
Given the ER difficulties that youth with anxiety in improving emotion regulation in youth with
disorders display, investigators have begun test- anxiety disorders (Suveg et al., 2009); nonethe-
ing the potential benefits of including ER content less, CBT does include strategies that target emo-
into treatment for youth with anxiety disorders tion regulation (e.g., relaxation). Further, the use
(Kennedy et al., 2019; Suveg et al., 2018). For of a much larger sample size in the RCT, in com-
instance, given a robust body of literature sup- parison to prior work, may have allowed for a
porting cognitive-behavioral therapy (CBT) for more rigorous test of hypotheses.
the treatment of anxiety disorders in youth Given the robust body of literature highlight-
(Comer et al., 2019), investigators have incorpo- ing ER deficits as central to many psychological
rated additional treatment components that disorders, including anxiety disorders, investiga-
address broad emotion-related deficits identified tors have turned to transdiagnostic treatment
in youth with anxiety disorders (e.g., emotion- approaches which aim to target proposed under-
focused CBT (Suveg et al., 2018)). Emotion- lying transdiagnostic risks or mechanisms of
focused CBT (ECBT) aims to improve emotion pathology. As one example, the Unified Protocol
understanding and regulation across a variety of (UP) is a transdiagnostic treatment approach that
emotions that a child may have difficulty regulat- was originally developed for the treatment of
ing. The first phase of ECBT focuses on identifi- emotional disorders in adults (UP; Barlow et al.,
cation of different emotions (e.g., anxiety, 2011), with downward extensions later devel-
sadness, pride, anger, guilt, happiness) and oped for adolescents (UP-A) and children (UP-C;
teaches youth how to recognize the emotion in Ehrenreich-May et al., 2018). UP focuses on core
oneself and others (e.g., how they are feeling, processes underlying a variety of emotional dis-
how they know they are feeling that way, why orders, including the notion that individuals with
they are feeling that way). Treatment exercises emotional disorders experience high levels of
are designed to engage the youth in discussion negative emotion and high emotional reactivity,
and other activities that facilitate reflection on which lead to poor emotion regulation skills (see
their emotional experiences. The second phase of Chap. 9 for a discussion of transdiagnostic mod-
treatment utilizes gradual exposure to anxiety- els of youth anxiety). A randomized controlled
provoking situations, as used in traditional CBT, pilot trial examined the efficacy of UP-C in the
with additional exposures to situations that pro- treatment of anxiety in a sample of 47 youth,
voke other emotions (e.g., anger, sadness). A aged 7–13 years, in comparison to an established
youth who typically has difficulty regulating anxiety-focused treatment (Cool Kids; Rapee
anger would engage in an exposure task designed et al., 2006). Results provided preliminary evi-
to elicit anger, to provide the youth with the dence that UP-C may be as efficacious in treating
opportunity, skills, and coaching to practice regu- anxiety as the established Cool Kids anxiety-
lating anger. focused treatment and may lead to even greater
Suveg et al. (2018) conducted a randomized improvement in aspects of emotion regulation
trial comparing traditional CBT to ECBT using a (Kennedy et al., 2019).
sample of 92 children (ages 7–12 years) with a Taken together, these studies examine how
primary anxiety disorder diagnosis (generalized inclusion of emotion regulation skills in treat-
anxiety disorder, social phobia, or separation ment may impact treatment outcomes. Continued
anxiety disorder). Both CBT and ECBT were research is necessary to further our understand-
effective in treating child anxiety symptoms, and ing of emotion regulation in youth with anxiety
both conditions showed similar improvements in disorders, with the goal of optimizing existing
emotion regulation and diagnostic and severity treatment programs.
Summary and Future Directions Becker, K. D., & Ginsburg, G. S. (2011). Maternal anxi-
ety, behaviors, and expectations during a behavioral
task: Relation to children’s self-evaluations. Child
Research has identified various ways in which Psychiatry and Human Development, 42, 320–333.
emotion dysregulation may be involved in the eti- Bender, P. K., Reinholdt-Dunne, M. L., Esbjørn, B. H.,
ology and maintenance of anxiety disorders in & Pons, F. (2012). Emotion dysregulation and
anxiety in children and adolescents: Gender differ-
youth. Some environmental and contextual fac- ences. Personality and Individual Differences, 53,
tors have been studied quite extensively (e.g., 284–288.
emotion socialization), yet there continues to be a Blackford, J. U., & Pine, D. S. (2012). Neural substrates
scarcity of research on the intersection of several of childhood anxiety disorders: A review of neuro-
imaging findings. Child and Adolescent Psychiatric
contextual factors including how culture influ- Clinics, 21, 501–525. https://doi.org/10.1016/j.
ences socialization, expression, and the use of ER chc.2012.05.002
strategies. The development of reliable and Blair, C., Ursache, A., & A. (2011). A bidirectional model
developmentally appropriate assessment tools of executive functions and self regulation. In K. D.
Vohs & R. F. Baumeister (Eds.), Handbook of self-
remains limited, so continued work in this area is regulation: Research, theory, and applications (2nd
necessary. CBT continues to be effective in treated., pp. 300–320). Guilford Press.
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nostic approaches are showing promise in E. K., Armstrong, J. M., Oler, J. A., et al. (2012).
Developmental pathways to amygdala-prefrontal
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ADs – such as emotion dysregulation. Overall, Nature Neuroscience, 15, 1736–1741.
continued work in this area will improve our Cannon, M. F., & Weems, C. F. (2010). Cognitive biases
understanding of ER in youth with anxiety disor- in childhood anxiety disorders: Do interpretive and
judgment biases distinguish anxious youth from their
ders and facilitate the optimizing and tailoring of non-anxious peers? Journal of Anxiety Disorders, 24,
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Chan, S. M., Poon, S. F. O., & Tang, E. M. H. (2016).
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Emergent Personality Features
in Adolescent Anxiety Disorders 14
Amanda Venta and Jaime L. Anderson
Introduction Personality disorders in the DSM-5 are

defined by pervasive and inflexible patterns of
Since the previous edition of this book was pub- feeling and behavior that onset in adolescence or
lished in 2011 (Johnson et al., 2011), the scien- early adulthood and lead to significant distress or
tific community has moved away from impairment (APA, 2013). Regarding traditional,
conceptualizing personality pathology only as categorical approaches to PD diagnosis, the
discrete diagnostic entities arranged into clusters DSM-5 includes ten PDs arranged into three
and toward dimensional, trait-based approaches clusters: Cluster A (odd-eccentric: paranoid,
that acknowledge issues of poor reliability, schizoid, and schizotypal PDs), Cluster B
comorbidity, and lack of specificity in personality (dramatic-emotional: antisocial, borderline, his-
disorder (PD) diagnoses. Indeed, whereas the trionic, and narcissistic PDs), and Cluster C
previous edition of the Diagnostic and Statistical (anxious- fearful: avoidant, dependent, and
Manual of Mental Disorders (DSM-4-TR; obsessive-compulsive PDs). This system has sig-
American Psychiatric Association [APA], 2000) nificant limitations including that what initially
relied exclusively on categorical classification of seem like discrete diagnostic entities are likely to
personality disorders (PDs), the latest edition be comorbid with one another (e.g., Kotov et al.
maintains the categorical diagnoses of DSM- (2017)) and, even within diagnoses, high hetero-
5-TR while adding an alternative, hybrid geneity is evident (e.g., Zimmerman et al.
dimensional/categorical model (DSM-5; APA, (2015)). Relatedly, DSM diagnoses, in practice,
2013). Though this chapter will address broad often evidence low reliability and provide little
personality features associated with anxiety dis- recourse for subthreshold presentations (Wall
orders in addition to the overlap with clinically et al., 2021). Finally, the DSM, particularly when
problematic PD, it is important to first address it comes to PDs, has been heavily focused on
shifts in the conceptualization and diagnosis of adults with little consideration of personality
psychopathology more broadly. pathology at other developmental stages.
In light of these criticisms, the scientific com-
A. Venta (*) munity has been moving toward dimensional
University of Houston, Department of Psychology, models for capturing psychopathology related to
Houston, TX, USA personality and otherwise. As noted, the DSM-5
e-mail: aventa@uh.edu includes an alternative model for PD (AMPD)
J. L. Anderson that conceptualizes PDs as a combination of
Sam Houston State University, Department of functional impairment (Criterion A) along with
Psychology & Philosophy, Huntsville, TX, USA
https://doi.org/10.1007/978-3-031-14080-8_14
204 A. Venta and J. L. Anderson
behavioral expressions or traits of personality els that may prove most useful in understanding
pathology (reflected in the model’s Criterion B). the overlap between anxiety and personality dys-
The trait model included in Criterion B asserts function. We then describe how these dimen-
that pathological personality traits fall within five sional models have conceptualized anxiety
empirically supported broad domains (negative psychopathology and focus on adolescents by
affectivity, antagonism, detachment, disinhibi- reviewing empirical research linking anxiety psy-
tion, and psychoticism), which roughly corre- chopathology with personality features and dis-
spond to pathological variants of the five-factor orders. Finally, we describe dimensional
model (FFM; APA, 2013). In addition, the most measures available for use in adolescents that are
recent version of the International Classification useful in examining anxiety and personality fea-
of Diseases (ICD-11; WHO, 2018) adopted a tures simultaneously, before closing with a chap-
new conceptualization of PDs that is dimensional ter summary.
in nature and characterizes personality pathology
as pervasive and distressing/impairing distur-
bance in self- and interpersonal functioning. Dimensional Conceptualizations
Though the core feature of PD diagnosis in the of Psychopathology
ICD-11 is functional impairment, this model also
includes a dimensional trait model. Similar to the The most prominent structural theories of psy-
DSM-5, this model includes five empirically sup- chopathology suggest that psychopathology is
ported dimensional trait domains (i.e., negative both dimensional and hierarchical. In other
affectivity, detachment, dissociality, disinhibi- words, lower-order symptoms of psychopathol-
tion, and anankastia). Each model reflects grow- ogy (e.g., distress, fear, impulsivity) are sub-
ing knowledge in the field that psychopathology sumed under broader higher-order domains (e.g.,
is likely best defined by dimensionally defined internalizing, externalizing). Though models of
traits or symptoms, rather than categories defined psychopathology have more recently been dis-
by symptom counts. cussed largely in their application to adult psy-
Alongside this shift in the diagnosis of PD, the chopathology, early dimensional and hierarchical
field has more broadly begun to steer away from conceptualization of mental health symptoms
reliance on categorical diagnoses. Though the was introduced in the child and adolescent litera-
DSM-5 remains the primary method of clinical ture. Achenbach (1966) identified two higher-
diagnosis, the DSM model is in contrast to most order domains of psychopathology in children,
psychopathology literature. Echoing these shifts labeled internalizing and externalizing, where
in the field, in preparing this chapter, we make a internalizing dysfunction included symptoms
deliberate move away from only discussing such as worrying, fear, and depression and exter-
comorbidity between anxiety and PDs as cate- nalizing dysfunction included symptoms such as
gorically defined entities and additionally focus disobedience, lying, and destruction. These
on how personality features, conceptualized in a higher-order domains continue to be replicated in
dimensional, trait-based approach, relate to anxi- child/adolescent research (e.g., Achenbach et al.
ety in adolescents. Indeed, we will argue that the (1991), Blanco et al. (2015), Lahey et al. (2004),
delineation between PD and what was previously and Lahey et al. (2008)).
termed “Axis I” psychopathology is quite vague Since this early work, structural research on
and that a focus on dimensional and hierarchical psychopathology has tended to focus more pre-
systems of psychopathology will better explain dominantly in the adult literature. Numerous
the overlap between these areas of dysfunction. studies have supported Achenbach’s model and
In order to lay the groundwork for the remain- identified both internalizing and externalizing
der of the chapter, we begin by describing con- factors in adults as well (e.g., Carragher et al.
temporary views on the structure of (2014), Krueger and Markon (2006), and Krueger
psychopathology, with a particular focus on mod- et al. (2005)). Broadly speaking, most models
14 Emergent Personality Features in Adolescent Anxiety Disorders 205
define internalizing dysfunction with symptoms underlying symptoms/traits account for variation
related to mood and anxiety and externalizing between them. Early work by Watson and
dysfunction with symptoms related to impulse Tellegen (1985) defined the nature of affective
control, antisocial behavior, and substance use. states, identifying two separate, but related,
Later work has also commonly identified a third dimensions (i.e., positive affect and negative
superspectrum in both adults and children, affect), wherein depressive symptoms are defined
termed thought dysfunction or psychosis (e.g., by low positive emotionality and anxiety symp-
Kotov et al. (2011a), Markon (2010), and Wolf toms are defined by high levels of negative affect.
et al. (1988)), with most hierarchical models of Following this, Clark and Watson (1991) intro-
psychopathology including each of these three duced the tripartite model, which asserted that
spectra at the highest order level. Notably, the there were three affective/internalizing domains.
exact hierarchy and structure of psychopathology These domains included physiological hyper-
vary between studies, with some suggesting an arousal (specific to anxiety), anhedonia (specific
optimal five-factor structure in which externaliz- to depression), and distress, wherein the latter
ing is bifurcated at a higher order level and social domain explained the existing overlap between
detachment forms its own domain (e.g., Kotov both anxiety and depressive disorders. This is
et al. (2017), Wright and Simms (2015)) or in consistent with later work on the structure of
which somatic symptoms form their own super- mood and anxiety, such as Sellbom et al. (2008)
spectrum (e.g., Kotov et al. (2011b), Marek et al. study identifying three similar domains repre-
(2020), and Sellbom (2017)). However, variation senting fear, distress, and low positive emotional-
understandably occurs based on the symptoms ity. Most reliably, however, the internalizing
measured or population studied, and the three superspectrum is found to bifurcate into two fac-
higher-order domains of internalizing, external- tors representing fear and distress, where distress
izing, and thought dysfunction are the most con- includes dysfunction such as depression and gen-
sistent findings at the broadest level. eralized anxiety and fear includes dysfunction
In addition to identifying the structure of psy- such as panic disorder and phobias (e.g., Eaton
chopathology at the broadest level, a large body et al. (2013), Krueger and Markon (2006)).
of research has also focused on the ways in which One of the most prominent (and growing)
these domains break down at lower levels (e.g., contemporary models of psychopathology comes
Kotov et al. (2011a), Clark and Watson (1991), from the Hierarchical Taxonomy of
Kotov et al. (2011b), Krueger (1999a), Krueger Psychopathology (HiTOP) consortium (Kotov
et al. (2007), Markon (2010), Sellbom et al. et al., 2017). This consortium of psychopathol-
(2008), Tellegen (1985), Tellegen et al. (1999), ogy experts was formed to consolidate the
Watson (2005), Watson and Tellegen (1985), research on dimensional systems and move the
Wright et al. (2013)). For instance, most models field forward in the application of such models.
of externalizing psychopathology bifurcate this Previous efforts have been limited by individual
domain into subfactors representing antagonism researchers or research groups working fairly
and disinhibition (e.g., Krueger et al. (2007)). independently to move this field forward (Kotov,
Most relevant to this chapter is the breakdown 2016). The HiTOP consortium provides a frame-
of the internalizing higher-order domain. Though work for the field to work together in better
a fair amount of work has modeled internalizing applying clinical science to clinical practice.
dysfunction as a unidimensional construct (e.g., Though the model is fluid and is intended to
Eaton et al. (2011), Fergusson et al. (2006), and change with the addition of new empirical evi-
Krueger et al. (1998)), there is substantial evidence, the current system includes six psychopa-
dence to support that this domain is hierarchical. thology “spectra,” termed internalizing,
In other words, an overarching internalizing disinhibited externalizing, antagonistic external-
dimension accounts for what is shared between izing, detachment, psychoticism, and somato-
disorders such as anxiety and depression, but form. These spectra are intended to provide
coverage of most areas of personality and psy- tural work on personality would suggest that both
chopathology, subsumed under one superspec- normal and pathological personality traits exist
trum representing a general factor of across domains of psychopathology. For instance,
psychopathology (Kotov et al., 2017). Of course, FFM neuroticism and ICD-11/DSM-5 negative
most relevant here is the internalizing domain, affectivity fall in a broad internalizing domain—
which includes subfactors of sexual problems, likely crossing between both fear and distress.
eating pathology, fear, distress, and mania (which Further, externalizing personality bifurcates into
also cross-loads onto thought disorder). domains generally representing antagonism and
In the HiTOP model (and most other dimen- disinhibition across personality models. Of
sional models), symptoms of anxiety fairly course, some personality traits are likely more
exclusively exist in two sub-domains (fear and relevant to anxiety than others. Personality
distress), with or without the inclusion of addi- traits—both normal and pathological—have been
tional subfactors. Consistent with previous litera- linked to anxiety in previous work (e.g., Clark
ture, the HiTOP fear subfactor includes social et al. (1994), Kotov et al. (2010), Widiger et al.
phobia, agoraphobia, specific phobia, social anx- (1999), and Widiger et al. (1999)), which will be
iety, panic disorder, and obsessive-compulsive reviewed throughout this chapter. For instance,
disorder, whereas the distress subfactor includes trait neuroticism is strongly tied to anxiety disor-
major depression, dysthymia, generalized anxi- ders (Bagby et al., 2017; Goldstein et al., 2018;
ety, post-traumatic stress disorder, and borderline Jeronimus et al., 2016), and some have argued
PD (Kotov et al., 2017). Therefore, there is a that it may even be the common feature across or
fairly reliable breakdown of anxiety disorders even predisposing factor for the development of
into the fear and distress domains. internalizing dysfunction (e.g., Griffith et al.
Generally speaking, PDs are more difficult to (2010), Tackett and Lahey (2017)). Although the
place in a particular domain or sub-domains. relationship between personality and psychopa-
Though previous iterations of the DSM have thology is complex, most contemporary models
relegated PDs to a separate axis entirely from that include both anxiety and PDs at minimum
that of other disorders, the reality is that person- show overlapping placement (e.g., Wright and
ality pathology is not so easily separated. Simms (2015)), such as placement of both gener-
Numerous personality and psychopathology alized anxiety disorder (GAD) and borderline PD
experts have asserted that personality and psy- (BPD) under the same subfactor in HiTOP (i.e.,
chopathology are inherently intertwined (e.g., distress; Kotov et al., 2017).
Krueger and Tackett (2003), Lengel et al. The sections that follow will discuss findings
(2016), Tackett and Mullins-Sweatt (2021), from previous research related to diagnostic
Widiger et al. (1999), and Widiger et al. (2019), comorbidity and personality correlates of anxiety
among others). Many have argued that personal- disorders in both adult and child/adolescent pop-
ity and psychopathology may even have a causal ulations. However, it is also important to keep in
relationship (e.g., Klein et al. (2011), Tackett mind when reviewing this work that separating
(2006), Tackett and Mullins-Sweatt (2021), personality from other areas of psychopathology
Widiger and Smith (2008)), which we explore is likely an impossible task. Most measures used
throughout this chapter, or that personality pro- to capture these constructs are not free from
vides the structural framework for other areas of influence of the other, and perhaps should not be,
psychopathology (Watson et al., 2016). Indeed, given the inherent link between personality and
Kotov et al. (2017) acknowledge the integral psychopathology. Further, most individuals
role of personality in establishing models of included in diagnostic research are not “pure”
psychopathology, including in the development cases of any type of psychopathology, and stud-
of the HiTOP model. ies that do screen for diagnostic purity are limited
In keeping with evidence that personality and in their application to natural settings in which
psychopathology are overlapping, most struc- comorbidity runs abound. As discussed in more
detail throughout the remainder of this chapter, suggests that personality and other forms of psy-
these relationships are complex, and contempo- chopathology are manifestations of the same
rary models may provide a better framework for continuum/continua. The research linking anxi-
understanding the ways in which personality and ety and personality pathology in youth has not
anxiety coexist. clearly converged on any one of these models.
We will refer back to these models throughout
this section to illustrate that point.
Anxiety and Personality
Anxiety and PD in Adults While our aim in
Importance of Comorbidity The previous iter- organizing this chapter is to highlight dimen-
ation of this chapter made a strong argument for sional conceptualizations of psychopathology
considering comorbidity between personality regarding PD and other symptomatologies—ado-
and anxiety disorders. Indeed, Johnson et al. lescent anxiety in our case—the reality is that
(2011) argued that consideration of comorbidity much extant literature examining links between
is important because (a) personality psychopa- personality and anxiety have relied on traditional,
thology may influence treatment progress and categorical conceptualizations of PD. This work
outcome for clients with anxiety symptomatol- has been foundational to the dimensional research
ogy and (b) the presence of maladaptive person- taking place today. Thus, we have elected to
ality features or PD can influence the course, include research linking anxiety with both PD
manifestation, and outcome of anxiety and personality features in this section. We will
disorders/symptoms and vice versa. For example, begin by reviewing evidence linking PD diagno-
PD diagnosis has been identified as a predictor of ses to anxiety.
poor response to both psychological and pharma-
cological interventions for people with anxiety Building upon early work supporting a link
disorders (e.g., Reich and Green (1991))—high- between anxiety and PD, Sanderson et al. (1994)
lighting the need to utilize instruments in clinical assessed a large sample of adults seeking outpa-
practice that address anxiety and personality fea- tient care for an anxiety disorder with the aim of
tures simultaneously. examining prevalence rates of PD across people
with anxiety disorders as a whole and within spe-
In youth, relations between personality and cific anxiety disorder categories. On a structured
psychopathology are perhaps more complex than clinical interview (i.e., structured clinical inter-
in adults because they reflect developmental tim- view for DSM-3/Axis II disorders, SCID-II), PD
ing effects as well as diagnostic comorbidity. was evident in more than a third (35%) of the
Tackett (2006) reviews four models explaining sample, with most of those disorders (27%)
links between personality and psychopathology reflecting Cluster C (anxious-fearful) PDs.
in development. (1) The complication or scar Indeed, avoidant PD, characterized by “a pattern
model posits that the development of, for exam- of social inhibition, feelings of inadequacy, and
ple, an anxiety disorder will change the individu- hypersensitivity” (APA, 2013), and obsessive-
al’s premorbid personality. (2) The pathoplasty or compulsive PD, “a pattern of preoccupation with
exacerbation model suggests that, in contrast, orderliness, perfectionism, and control” (APA,
premorbid personality may influence the “course, 2013), were the most prevalent PD diagnoses in
severity, presentation, or prognosis” of another their sample. The authors were careful to note,
disorder, like an anxiety disorder. (3) The vulner- however, that the link between Cluster C PDs and
ability or predisposition model hypothesizes that anxiety disorders is not unique, citing that 64%
premorbid personality traits put a child at risk of of patients with depressive disorders also met cri-
developing a particular constellation of patho- teria for a Cluster C PD (Sanderson et al., 1992).
logical symptoms, like those represented in the Instead, they suggest that the presence of Cluster
anxiety disorders. (4) Finally, the spectrum model C psychopathology predisposes subsequent
development of internalizing psychopathology instead demonstrating comorbidity with Cluster

broadly construed (in line with Tackett’s (2006) A (e.g., schizotypal) and Cluster B (e.g., border-
description of the vulnerability/predisposition line) personality pathology as well.
model).
Regarding anxiety disorders, participants with Anxiety and PD in Adolescents Turning our
social phobia and generalized anxiety disorder focus to youth, much about relations between
(GAD) in Sanderson’s study (1994) were the anxiety and personality pathology can be learned
most likely to meet diagnostic criteria for a from the longitudinal Children in the Community
comorbid PD, occurring in 61% and 49% of Study which followed nearly 1000 youth across
those clients, respectively. The authors speculate 10 years (Cohen & Cohen, 1996). In a subset of
that these two anxiety disorders, like depressive more than 700 youth, Goodwin et al. (2005)
disorders, have “pervasive effects on personality” reported that the prevalence of panic attacks, a
(pg. 171), perhaps explaining the particularly symptom and correlate of numerous anxiety dis-
strong link to PD among clients with those two orders, when subjects were, on average, 13 years
disorders. Regarding GAD specifically, they old, was associated with higher rates of PD 10
argue that perhaps this disorder is better concep- years later, even after controlling for demo-
tualized as a PD than an anxiety disorder due to graphic variables, adolescent PD, and other
the lifelong and chronic course. This argument comorbidities. Panic attacks increased the odds
calls to mind Tackett’s (2006) description of the of a future Cluster A personality diagnosis most
spectrum model as well as the HiTOP model, steeply but also increased risk for Cluster B and
suggesting that perhaps GAD lies on a continuum Cluster C diagnoses. The authors speculate that
with various forms of personality pathology. In adolescent panic attacks could act as a risk factor
contrast, individuals with specific phobia were for subsequent PD diagnosis (indicative of
less likely to be diagnosed with a PD (12%). Tackett’s (2006) vulnerability model) or could
While this study was conducted in adults (and reflect a “prodromal stage of the onset of a per-
found no relation between the presence of anxi- sonality disorder” (p. 231), suggesting a spec-
ety-PD comorbidity and age), it set the stage for trum model is at play. Alternatively, they suggest
future research to be undertaken with adolescents that panic attacks may actually lead to the devel-
by demonstrating the sheer prevalence of person- opment of PD, in particular avoidant PD, due to
ality pathology in anxious clients. Sanderson the adversity of experiencing panic attacks in
et al. (1994) also lay the groundwork for the social settings (suggesting a complication or scar
dimensional conceptualizations of psychopathol- model; Tackett, 2006).
ogy we have already reviewed and the research
linking dimensional conceptualizations of mal- Further, Kasen et al. (1999) also utilized data
adaptive personality to anxiety disorder that we from the Children in the Community Study to
will review in subsequent sections, by putting examine how anxiety pathology (among other
forth an argument (and data) that blurs the lines forms of psychopathology) in youth ages 9–16
between anxiety and PD (i.e., suggesting that years (N = 551) related to PD over the next 10
GAD be conceptualized as a PD). Further, they years. Approximately, 15% of their sample had
note that the prevalence rates of PD in their sam- experienced an anxiety disorder by the age of 18
ple differ from other studies, even those that used years, and the presence of an anxiety disorder
similar samples and assessment instruments, sug- increased the odds of a PD in young adulthood.
gesting that lack of reliability in PD diagnosis Specifically, anxiety disorder (i.e., separation
may be to blame. It is important to note that both anxiety disorder and social phobia) increased the
in Sanderson and colleagues’ (1994) work and in odds of Cluster A PD fivefold and Cluster C per-
a seven-year longitudinal study conducted by sonality fourfold. Effects were exacerbated when
Ansell et al. (2011), anxiety disorders were not PD was also present in youth, though predictive
exclusively associated with Cluster C PDs, effects persisted even after controlling for youth
PD. In line with a vulnerability or predisposition adolescents. Indeed, a study of inpatient adoles-
model moving from anxiety to personality pathol- cents with BPD (reflecting instability in interper-
ogy, the authors posit that the presence of either sonal relationships, self-image, and affect as well
of the two anxiety disorders considered in their as impulsivity; APA, 2013) indicated that 63% of
study may deter and restrict social involvement, the BPD group also met diagnostic criteria for an
reinforcing social avoidance and arresting social anxiety disorder—actually exceeding the rate of
development until it emerges as “traitlike pathol- depressive disorders in their sample (61%; Sharp
ogy” (p. 1533) reflected in Cluster A and C PDs. et al., 2012). Similarly, Chanen et al. (2007)
Other longitudinal researches also confirm found that the presence of any anxiety disorder
links between anxiety and maladaptive personal- was significantly associated with BPD diagnosis
ity in youth. For instance, Lewinsohn et al. (1997) in a sample of psychiatric outpatients ages 15–18
examined the prevalence of anxiety disorders, years. Importantly, though, anxiety disorder was
among other forms of psychopathology, in almost also associated with other PDs, such that the
300 adolescents (ages 14–18) and again at age 24 prevalence of anxiety in the BPD group (45.7%)
years. In this study, anxiety disorders in adoles- was significantly higher than in the other PD
cence were among the diagnostic categories most group (36.4%), but the prevalence in the other PD
closely associated with later personality pathol- group was significantly higher than in the no PD
ogy. Indeed, anxiety in adolescence was associ- group (18.6%). This work echoes much of the
ated with increased risk for avoidant, borderline, aforementioned longitudinal research showing
dependent, histrionic, paranoid, schizoid, and that anxiety is associated with personality pathol-
schizotypal PDs. Even after adjusting for demo- ogy in general, rather than one specific form of
graphic variables, depression, and other psycho- anxiety disorder predicting one specific form of
pathologies, anxiety remained associated with personality pathology.
avoidant, borderline, dependent, schizoid, and
schizotypal PDs—more than any other form of Negative Emotionality The Dunedin
psychopathology considered (i.e., major depres- Multidisciplinary Health and Development Study
sive disorder, disruptive behavior, and substance (Silva, 1990), a longitudinal study beginning in
use). The strongest associations were reported age three with assessments throughout adoles-
between anxiety and schizotypal and schizoid cence and young adulthood, has provided valu-
PDs. The findings of this study and others able longitudinal data on the relation between
(Bernstein et al., 1996; Rey et al., 1995) speak anxiety and personality pathology when concep-
clearly to a link between anxiety psychopathol- tualized dimensionally. Their findings have been
ogy in adolescence and personality pathology but instrumental in identifying negative emotionality,
should not necessarily be interpreted as evidence a personality dimension similar to neuroticism
of causality/directionality. Indeed, longitudinal reflecting a propensity to experience and react to
data from Johnson et al. (1999), also based on the negative emotions, as a correlate of anxiety.
Children in the Community Study, linked PD in
adolescence to anxiety (and other) disorders in In nearly 900 participants, Krueger et al.
youth suggesting bidirectional links between (1996) examined personality pathology dimen-
these two diagnostic categories. Consistent with sionally, utilizing the Multidimensional
a pathoplasty or exacerbation model, PD in ado- Personality Questionnaire (MPQ), among
lescence, in some instances, was associated with 18-year-old participants, in relation to anxiety
increased severity of psychopathology in young disorders (among other forms of psychopathol-
adulthood, as reflected in suicidal behavior. ogy) determined by structured interview con-
Concurrent research, which examines correla- ducted when participants were 15 years old and
tions between personality and anxiety disorders also at 18 years of age. Their concurrent data
at one point in time, also highlights comorbidity revealed that individuals (aged 18) who were
between personality and anxiety disorders in diagnosed with an anxiety disorder experienced
lower agency and communion scores and higher extraversion. As we saw in the previous section,
negative emotionality scores on the high neuroticism (or negative emotionality) has
MPQ. Similarly, anxiety symptoms at age 15 been repeatedly associated with internalizing
were associated with lower agency, lower com- psychopathology, generally, and anxiety pathol-
munication, and greater negative emotionality on ogy, specifically, in adolescents. Extraversion,
the MPQ at 18 years of age. However, the authors reflecting the quantity and intensity of an indi-
suggested that many of the relations between per- viduals’ interpersonal interactions and positive
sonality and anxiety observed in their work are emotions, has likewise been associated with anx-
best explained by comorbidity because they dis- iety disorders repeatedly in adult samples
appeared when examining participants with (Brandes & Bienvenu, 2006). In this section, we
“pure anxiety” (i.e., anxiety disorder and no other review the corollary of extraversion among
forms of psychopathology). One facet of negative youth—behavioral inhibition—in relation to anx-
emotionality on the MPQ, stress reaction, how- iety disorders in youth.
ever, retained a relation to “pure anxiety.” The
authors suggested that perhaps this aspect of neg- In children, many studies have linked behav-
ative emotionality “may contribute to determin- ioral inhibition with increased likelihood of
ing the precise form that maladaptation takes” developing an anxiety disorder (see Oosterlaan
(p. 310), with the stress reaction facet pointing in (2001) for a review) and suggested that tempera-
the direction of internalizing disorder and aggres- mental over-inhibition, consistent with a vulner-
sion (another facet of negative emotionality) pre- ability or predisposition framework, acts as an
dicting externalizing disorder. etiological factor for later anxiety disorder.
Krueger (1999a, b), also utilizing data from Several studies have also linked behavioral inhi-
the Dunedin study, demonstrated that the links bition with anxiety in adolescent age groups.
between anxiety and personality pathology are Oldehinkel et al. (2004), for example, examined
also bidirectional. Indeed, this second study indi- more than 2200 10- to 12-year-olds living in the
cated that personality traits in adolescence are Netherlands and participating in a prospective,
associated with anxiety disorder in young longitudinal study. Utilizing continuous rating
adults—again featuring negative emotionality scales of psychopathology and temperament,
prominently. In particular, high negative emo- they linked decreased surgency (which can be
tionality in late adolescence was associated with thought of as increased behavioral inhibition)
anxiety, as well as other forms of psychopathol- and other personality traits with increased likeli-
ogy, at age 21 years, even after controlling for hood of internalizing symptoms. They posited
other psychopathologies in adolescence. Beyond that while degree of surgency influenced the like-
the Dunedin sample, several other studies have lihood of an adolescent developing internalizing
confirmed links between negative emotionality (low surgency) versus externalizing problems
(or neuroticism) and anxiety pathology in adoles- (high surgency), negative affectivity explained
cence (see Tackett (2006)). the severity of maladaptive functioning overall.
Though ample research, like Oldehinkel et al.
Behavioral Inhibition Behavioral inhibition, (2004), has linked behavioral inhibition in child-
while not truly a personality trait, is a tempera- hood to a number of pathological outcomes, most
mental dimension that has been repeatedly asso- notably in the internalizing domain, it is one tem-
ciated with anxiety symptoms and disorders in peramental domain in which there is some evi-
youth and therefore bears some discussion. The dence of specificity with anxiety disorder. That
initial definition of behavioral inhibition by is, Hirshfeld-Becker et al. (2008) summarize
Kagan et al. (1984) centered on the tendency to decades of research saying “Prospective longitu-
withdraw or show reluctance or fear in new situ- dinal studies of children with BI [behavioral inhi-
ations. In Tackett’s (2006) taxonomy, behavioral bition] from five different high-risk and
inhibition reflects high neuroticism and low community samples have found that in early and
middle childhood and adolescence, inhibited scales have had substantial empirical support
children have elevated rates of anxiety disorders” (e.g., De Moor et al. (2009), Jackson and Trull
(p. 361). Further, they review studies indicating (2001), Stein et al. (2007), and Walters (2007)).
that behavioral inhibition is specifically associ- Furthermore, research has demonstrated the util-
ated with risk for social anxiety in adolescence ity of the PAI more broadly in assessing PD
(with evidence of this association in childhood as (Bradley et al., 2007; Oltmanns et al., 2016),
well), suggesting a more specific relation between including from a DSM-5 AMPD perspective
these two domains of pathology than has been (Busch et al., 2017; Hopwood et al., 2013).
evidenced in the other research reviewed in this Indeed, although focused on the adult version of
section. the instrument, this research has demonstrated
conceptually expected overlap between anxiety
symptoms and personality psychopathology.
Measurement of Psychopathology Therefore, scales on the PAI-A are likely to pro-
vide excellent coverage of anxiety problems
To end this chapter, we will briefly discuss the along with some of the most common and prob-
ways in which psychopathology is measured in lematic symptoms of personality dysfunction.
adolescents, with a particular focus on instru- The MMPI-A similarly includes several scales
ments that include an assessment of both anxiety to assess the anxiety-related problems. Perhaps
and personality psychopathology. As discussed most compelling is that this measure includes
throughout the course of this chapter, the differ- five Personality Psychopathology-Five (PSY-5)
entiation between anxiety disorder and PD is not scales, which were derived to assess five broad
completely clear, and the role one plays in the pathological traits (neuroticism/negative emo-
development of the other remains undecided. tionality, introversion/low positive emotions, dis-
Measures that assess anxiety are likely to tap into constraint, psychoticism, and aggressiveness). In
some level of personality dysfunction and vice their adult version on the MMPI-2-RF (Tellegen
versa; however, measures that explicitly assess & Ben-Porath, 2008/2011), research has shown
both personality dysfunction and anxiety symp- strong convergence between these scales and
toms may be optimal. both the DSM-5 and ICD-11 trait models (e.g.,
Two measures that explicitly include coverage Anderson et al. (2013), Sellbom et al. (2020)).
of both anxiety and personality dysfunction are The more recent MMPI-A-RF also includes
the Personality Assessment Inventory-Adolescent revised PSY-5 scales. Furthermore, it was restruc-
(PAI-A; Morey, 2007) and Minnesota Multiphasic tured similarly to the MMPI-2-RF, which not
Personality Inventory-Adolescent/Adolescent-only made psychometric improvements but also
Restructured Form (MMPI-A/MMPI-A-RF; purposefully organized the instrument that con-
Archer et al., 2016; Butcher et al., 1992). These verges with hierarchical and dimensional models
measures each have a fair amount of stand-alone of psychopathology (Sellbom, 2017; Sellbom,
empirical support but also benefit by being 2019). Indeed, similar to the tripartite model of
adapted from their adult equivalent measures, depression and anxiety (Clark & Watson, 1991),
which are widely used and supported in clinical internalizing psychopathology divides into scales
practice as well as heavily researched. The PAI- representing fear, distress, and low positive emo-
A, appropriate for adolescents ages 12–18, tionality (Sellbom et al., 2008). Not surprisingly,
includes scales reflective of generalized anxiety, scales representing symptoms of anxiety have
phobias, trauma, and obsessive-compulsive shown strong correlations with relevant patho-
symptoms, with independent empirical support logical personality traits (Anderson et al., 2015;
of their construct validity (Vanwoerden et al., Anderson & Sellbom, 2021; Tarescavage &
2018). In addition, this measure includes specific Menton, 2020). Though much of this work is
evaluation of both borderline and antisocial focused on the adult version of the instrument, it
PD. The PAI (Morey, 1991) versions of these is likely that the adolescent version of these
scales would show similar relationships. Indeed, Anderson, J. L., & Sellbom, M. (2021). Assessing ICD-
11 personality trait domain qualifiers with the MMPI-
the MMPI-A-RF is likely to provide optimal cov- 2-RF. Journal of Clinical Psychology, 77, 1090–1105.
erage of both anxiety and personality psychopa- Anderson, J. L., Sellbom, M., Bagby, R. M., Quilty, L. C.,
thology in a manner consistent with contemporary Veltri, C. O. C., Markon, K. E., & Krueger, R. F.
movements in the field. (2013). On the convergence between PSY-5 domains
and PID-5 domains and facets: Implications for
assessment of DSM-5 personality traits. Assessment,
20(3), 286–294.
Chapter Summary Anderson, J. L., Sellbom, M., Bagby, R. M., Ayearst,
L., Quilty, L. C., & Chmielewski, M. S. (2015).
Associations between DSM-5 section III personal-
In this chapter, we make a deliberate move away ity traits and the Minnesota Multiphasic Personality
from discussing comorbidity between anxiety Inventory 2-Restructured Form (MMPI-2-RF)
and PDs only as categorically defined and instead scales in a psychiatric patient sample. Psychological
add recent research regarding how personality Assessment, 27(3), 801–815.
Ansell, E. B., Pinto, A., Edelen, M. O., Markowitz, J. C.,
features, conceptualized in a dimensional, trait- Sanislow, C. A., Yen, S., et al. (2011). The association
based approach, relate to anxiety in adolescents. of personality disorders with the prospective 7-year
This move reflects a broader shift in the science course of anxiety disorders. Psychological Medicine,
of PD, away from categorical approaches and 41(5), 1019.
Archer, R. P., Handel, R. W., Ben-Porath, Y. S., &
toward dimensional models that better capture Tellegen, A. (2016). Minnesota Multiphasic
the overlap between PD categories and other Personality Inventory-Adolescent-Restructured Form
forms of psychopathology. We discussed dimen- (MMPI-A-RF): Manual for administration, scoring,
sional conceptualizations of psychopathology, interpretation, and technical manual. University of
Minnesota Press.
and we reviewed longitudinal and cross-sectional Bagby, R. M., Uliaszek, A. A., Gralnick, T. M., &
empirical research linking anxiety psychopathol- Al-Dajani, N. (2017). Axis I disorders. In T. A.
ogy with personality features and diagnoses. Widiger (Ed.), The Oxford handbook of the five factor
Finally, we discussed measures that can be used model (pp. 479–506). Oxford University Press.
Bernstein, D. P., Cohen, P., Skodol, A., Bezirganian, S., &
with adolescents to examine anxiety and person- Brook, J. S. (1996). Childhood antecedents of adoles-
ality features simultaneously, recognizing the cent personality disorders. The American Journal of
reality that these forms of pathology are not as Psychiatry, 153(7), 907–913.
distinct as we once believed. Blanco, C., Wall, M. M., He, J. P., Krueger, R. F., Olfson,
M., Jin, C. J., et al. (2015). The space of common psy-
chiatric disorders in adolescents: Comorbidity struc-
ture and individual latent liabilities. Journal of the
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Family Components of Child
Amanda Palo and Abigail Candelari
The relationship between the parenting environ- pathology, underscoring the need to study other
ment and the development and maintenance of layers of risk, including family factors and the
anxiety disorders has received substantial scien- family environment.
tific attention for the past four decades (Last Studies assessing the prevalence of anxiety
et al., 1987). The present chapter outlines the cur- disorders among families reveal up to seven times
rent state of knowledge regarding family factors higher rates of anxiety disorders among children
and their relationship to childhood anxiety, start- of clinically anxious parents, compared to fami-
ing with historical context and a summary of tra- lies in which no family members have problem-
ditional theoretical models. Finally, a review of atic anxiety symptoms (e.g., Biederman et al.
the progress made by more recent literature is (1991), Last et al. (1987), and Turner et al.
presented. (1987)). These results have been replicated in
Childhood anxiety disorders have unique tem- both small and large samples, and findings have
peramental underpinnings (Caspi et al., 1995; remained consistent over time as genetic study
Crawford et al., 2011). For example, biologically methodology advances (Telman et al., 2018).
based differences in emotional reactivity predict Although these studies provide useful insight on
childhood internalizing symptoms (Caspi et al., the heritability of anxiety, they do not explain the
1995; Eisenberg et al., 2017), and having a diffi- specific relative contributions (i.e., amount of
cult temperamental profile (i.e., slow adaptabil- variance) of genetic and environmental factors or
ity, high affective intensity, and negative the mechanisms by which the family environ-
emotionality (Bates, 1980)) has been found to ment may maintain or exacerbate anxiety. Taken
predict onset of anxiety symptoms (Miner & together, etiological models of anxiety must con-
Clarke-Stewart, 2008). Yet, not all children with sider other transdiagnostic factors that contribute
difficult temperaments develop internalizing to risk.
Given the universally central role of the fam-
A. Palo (*) ily environment among children (Henderson &
Department of Psychiatry and Behavioral Sciences, Berla, 1994), researchers have studied family
Baylor College of Medicine, Houston, TX, USA factors that may elucidate the development of
e-mail: amanda.palo@bcm.edu child anxiety for over four decades. In the follow-
A. Candelari ing sections, we summarize the findings of this
Department of Psychiatry and Behavioral Sciences, literature, including problematic parenting
Baylor College of Medicine, Houston, TX, USA
behaviors and temperamental vulnerabilities that
Department of Psychology, University of Houston, may contribute to onset of anxiety among youth.
Houston, TX, USA
https://doi.org/10.1007/978-3-031-14080-8_15
218 A. Palo and A. Candelari
Review of Literature and cope are increased, which facilitates devel-

opment of autonomy (Ollendick & Grills, 2016).
The parenting environment has a robust role in Learning to self-regulate in the context of experi-
the development of childhood internalizing encing difficult emotions facilitates worldviews
symptoms (Cummings et al., 2003; Jaffee et al., in which conflicts are solvable and challenges
2002). A review of landmark studies in the 1990s can be overcome. Finally, environments that
(Wood et al., 2003) and more recent reviews teach the value in attempting to problem-solve
exploring the parenting environment of clinically can provide the opportunity for increased per-
anxious youth have consistently identified paren- ceived mastery over situations (including diffi-
tal overcontrol and modeling of anxious behav- cult ones), thereby encouraging children to
iors as key in the development and maintenance approach opportunities to problem-solve, rather
of childhood anxiety symptoms (McLeod et al., than avoid them.
2007; Ollendick & Benoit, 2012). A recent population-based study found that
among preschool-aged behaviorally inhibited
children, parent’s mental health, harsh discipline,
Maternal Overcontrol and overcontrolling parenting practices were sig-
nificantly associated with the likelihood of hav-
Maternal overcontrol (also known as overprotec- ing an anxiety disorder by age 5 years, with
tion, intrusiveness, overinvolvement, or psycho- maternal overcontrol the strongest predictor of
logical control in the literature) is characterized these three (Bayer et al., 2019). In this longitudi-
by excessive regulation of the activities of youth, nal investigation, approximately half of behavior-
intrusive parental overprotection, and intrusive ally inhibited youth developed a clinical level of
influence on youths’ decision-making. Maternal anxiety by the age of six (Bayer et al., 2019).
overcontrol also includes influencing children’s Traditionally in the literature, constructs
natural emotional reactions with instructions on including parental overcontrol, overintrusive-
how to feel or what to think in situations (espe- ness, overinvolvement, and overprotection were
cially situations characterized by difficult emo- grouped together as one construct (McLeod et al.,
tions; Barber (1996) and Barber et al. (2012)). 2007; van der Bruggen et al., 2008). More
Compared to mothers of nonanxious children, recently, evidence suggests that the specific type
mothers of clinically anxious children demon- of controlling parental behavior matters.
strate more overcontrolling behaviors, solicit Psychological control refers to parenting tech-
children’s ideas less, and are less likely to accept niques including guilt or shaming in response to
children’s opinions (Moore et al., 2004; Siqueland the child not behaving according to parental
et al., 1996; Whaley et al., 1999). expectations (Barber & Harmon, 2002).
Maternal overcontrol is problematic in the Consistent with traditional (behavioral) concep-
context of childhood anxiety because when par- tualizations of maternal overcontrol, psychologi-
ents encourage reliance on adults for information cal overcontrol appears to reduce perceived
on how to feel and what to do in difficult situa- mastery, potentially leading to perceived help-
tions, perceived mastery over children’s own lessness and lack of mastery over the environ-
environments is gradually diminished. Lack of ment (perspectives known to be associated with
mastery over the environment is linked to a cog- internalizing symptoms (Garber & Flynn, 2001)).
nitive bias for interpreting everyday events as out Pinquart (2017) conducted a meta-analysis of
of their control (Chorpita & Barlow, 1998), which 1015 studies, of which 344 included assessments
is associated with cognitive biases relevant in of behavioral overcontrol and 163 included psy-
anxiety disorders. Research suggests that when chological control. Results indicated that behav-
children are in environments that allow them to ioral control was associated with lower
navigate their own decisions, including in chal- internalizing symptoms, while psychological
lenging situations, opportunities to self-regulate control was related to increased internalizing
15 Family Components of Child and Adolescent Anxiety Disorders 219
symptoms with very small to small effect sizes. utes following exposure to the negatively paired
Of note, baseline child anxiety predicted stimulus. Although cross-sectional in nature, this
increases in psychological control and declines in study demonstrated that a mother’s affective
warmth, providing evidence for bidirectional response toward novel stimuli has a clear impact
influences within the parent-child relationship. on her infant’s subsequent behavior toward that
Neglectful and authoritarian parenting prac- stimulus. These findings have been replicated in
tices (each characterized by low parental warmth similar experimental designs showing that mater-
(Maccoby & Martin, 1983)) were associated with nal avoidance of distressing stimuli (e.g., spiders)
elevated levels of internalizing symptoms, while moderates the relationship between fear of cer-
permissive parenting was not significantly related tain stimuli in mothers and children (Askew
(Pinquart, 2017). The authors hypothesize that et al., 2014; Lebowitz et al., 2015).
low parental warmth may explain the increases in Another experiment examining maternal anxi-
internalizing symptoms, and given lack of any ety and maternal emotion regulation during a dis-
observed deficits in parental warmth in permis- tressing task where mothers listened to an audio
sive parenting, it is possible that the negative recording of a child in distress pleading for help
effects of lack of parental behavioral control may found that displays of maternal anxiety predicted
be compensated by positive effects of parental ineffective maternal emotion regulation during
warmth. the exposure task, which in turn predicted greater
maternal accommodation and higher child anxi-
ety (Kerns et al., 2017). This finding suggests that
arental Modeling of Anxious
P displays of ineffective emotion regulation may
Behaviors mediate the relationship between maternal and
child anxieties.
The cognitive model of anxiety posits that cogni-
tive misinterpretations lead to an exacerbation of
anxiety symptoms via disrupted or inaccurate Temperament and Parenting
thinking patterns, and a large body of work has
shown that cognitive risk factors for anxiety Temperament refers to heritable and moderately
aggregate within families (Biedel & Tuner, 1997; stable traits that serve as the “building blocks”
Last et al., 1987). Fortunately, children can learn for adult personality (Auerbach et al., 2008;
to regulate their own thoughts – however, this Rothbart 1981). Temperament is a robust predic-
depends largely on learning experiences, which tor of later personality traits (e.g., impulsivity,
typically occur in the presence of parents. Several extraversion (Rothbart et al. 2000a, b)), even
lines of research in parenting and anxiety have after accounting for gender and socioeconomic
suggested that parents’ own modeling of anxious status. Infant temperament demonstrates moder-
behaviors increases the likelihood of children ate stability and continuity into middle childhood
cognitively misappraising a situation. This is (Carey & McDevitt, 1978; Rothbart et al., 2000a,
problematic, given that anxious children are b), and its role in the emergence of anxiety symp-
already prone to cognitive biases which overesti- toms has been of considerable scientific interest
mate the actual level of danger in a given situa- for decades (Goldsmith & Campos, 1982).
tion. These cognitive biases are related to Behavioral inhibition (BI) refers to a tempera-
subsequent anxiety manifestations (Chorpita mental trait characterized by fear and apprehen-
et al., 1996; Micco & Ehrenreich, 2008). sion in novel situations (Degnan et al., 2008). BI
For example, Gerull and Rapee (2002) found has been shown to predict anxiety symptom
that toddlers showed greater fear and avoidance severity over time (Mian et al., 2011) as well as
of an aversive stimulus when mothers showed a anxiety disorders in general (Biederman et al.,
negative reaction. After seeing their mother’s 2001; Turner et al., 1996; van Brakel et al., 2006)
reaction, avoidance was observed up to 10 min- and particularly social anxiety disorder
(Chronis-Tuscano et al., 2009; Muris et al., and anxiety are separate constructs. To illustrate,
2011). The parenting environment is thought to BI is associated with chronic and excessive
interact with temperamental risk factors like arousal and avoidance, and an insecure attach-
behavioral inhibition and level of emotional reac- ment is associated with frustration intolerance,
tivity. Children high in temperamental traits such difficulty being soothed, and distress when faced
as frustration and impulsivity, yet low in effortful with novel situations (Manassis, 2001) – all char-
control, are more vulnerable to the adverse effects acteristics of anxiety disorders.
of negative parenting and elicit parental responses In light of these challenges and limitations,
that reinforce such traits (Kiff et al., 2011). temperament and parent/child attachment bonds
Research has also found that among children remain important constructs to consider when
with temperamental profiles characterized by evaluating risk level for anxiety. Childhood
high reactivity and negative emotionality, adap- behavioral inhibition and signs of an insecure
tive behavioral development depends, in part, on attachment signal future risk for an anxiety disor-
their experiences with caregivers (Wachs, 2000). der. Indeed, there is emerging evidence that chil-
For instance, children with high negative emo- dren with BI respond to early intervention
tionality are more likely to exhibit elevated anxi- strategies aimed at reduction of anxiety symp-
ety symptoms if their mothers react with toms (Rapee et al., 2005) and that improving the
disproportionately high sensitivity to the child’s quality of the parent-child attachment relation-
behaviors (Davis et al., 2015). Likewise, parental ship may also be effective in minimizing internal-
overprotection and overcontrolling behaviors are izing anxiety symptoms (Choate et al., 2005;
associated with increased internalizing problems Siqueland et al., 2005).
(Bayer et al., 2019; McLeod et al., 2007), partic- The literature to date focusing on the link
ularly among youth high in behavioral inhibition. between parenting and child anxiety has provided
Manassis and Bradley (1994) proposed a theo- important insights and advanced our theoretical
retical model in which temperament and parent- understanding of this relationship, and modern
child attachment both equally confer risk for the multimodal studies have advanced our under-
development of childhood anxiety, but the level standing of the transactional nature of child and
of risk is greater for children who have both BI parent behaviors. Still, this literature base has a
and an insecure attachment bond with the care- number of important limitations (Lawrence et al.,
giver. Unfortunately, the relationship among 2019; McLeod et al., 2011). First, studies vary
these and other risk factors remains poorly significantly in the operationalization of parent-
understood. ing constructs studied, which has made it difficult
Notable limitations of this body of literature to compare results across studies. In addition,
include the absence of data on the directionality relatively little attention has been paid to the rela-
of the relationships and overlap between con- tionship between parenting behaviors and the
structs. It is likely that factors unique to each development of specific anxiety disorders, as
child, such as temperament, personality, and anx- opposed to more general measures of anxiety.
iety expressed to the parent, shape parenting Research in this area can help identify risk fac-
behaviors and ultimately the attachment relation- tors for specific anxiety disorders in youth and
ship (Hudson et al., 2009; Moore et al., 2004; can inform prevention and treatment interven-
Whaley et al., 1999). One mechanism of how tions. Further, there is a long-standing focus on
parenting may contribute to child internalizing the behavior of mothers within the research base,
problems is lack of opportunities to face and such that comparatively little is known about the
overcome fears, and parents of shy/inhibited chil- importance of fathers’ behaviors when it comes
dren likely mean well when they attempt to shel- to the development of child and adolescent anxi-
ter their child from the potential for failure. In ety disorders. In terms of identifying causal links,
addition, it is important to consider the extent to the literature base would benefit from increased
which BI, difficulties with insecure attachment, use of experimental studies, especially more
longitudinal experimental designs (McLeod on fathers’ overcontrolling behaviors, with mixed

et al., 2011). Importantly, there has also been dif- findings. Specifically, some studies suggest that
ficulty assessing developmental considerations paternal overcontrol (but not maternal overcon-
related to the appropriateness of specific parent- trol) is associated with increased anxiety in
ing behaviors based on the age of the child (e.g., infants (Moller et al., 2015), middle-aged chil-
more parental control and involvement may func- dren (Pereira et al., 2014), and adolescents, with
tion differently with preschoolers as compared to this association being stronger among older ado-
adolescents), and studies have focused heavily on lescents in particular (Verhoeven et al., 2012). In
adolescents. The childhood anxiety literature has contrast, others have found no association
traditionally focused heavily on middle child- between paternal anxiety or paternal parenting
hood to adolescence because anxiety commonly behaviors and child social anxiety symptoms
emerges during the teenage years; however, there (Bogels et al., 2001). For instance, Verhoeven
is currently a particular need to assess parental et al. (2012) found that among 8- to 12-year-old
behaviors that promote adaptive emotion regula- children, paternal overcontrol did not signifi-
tion during the early childhood years (i.e., teach- cantly predict child anxiety symptoms, whereas
ing language for expression of emotions, emotion maternal overcontrol did.
coaching (Roben et al., 2013)). Since the first Others have examined the parenting behaviors
edition of this text, the literature has moved to of anxious fathers in particular to determine the
address some of these limitations; what follows is extent to which they engage in parenting behav-
a discussion of the role of fathers in the develop- iors that are associated with child anxiety. Teetsel
ment of child anxiety disorders, the association et al. (2014) found that among a sample of non-
between parenting behaviors and the develop- anxious children, fathers with a DSM-IV anxiety
ment of specific anxiety disorders, and discussion diagnosis demonstrated more controlling behav-
of challenging parenting behavior, a relatively iors (e.g., intrusive and unsolicited help, complet-
new construct. ing the task for the child, over-instructing the
child) than anxious mothers during a difficult
parent-child laboratory task. In contrast, anxious
Fathers and Child Anxiety Disorders fathers demonstrated less reinforcement of the
child’s dependence on his/her parent and utilized
Historically, the vast majority of the research less punishment than anxious mothers. Of note,
examining parenting and child anxiety symptoms these researchers found no difference between
has focused on mothers (Bogels & Phares, 2008; the levels of autonomy-granting behaviors,
Teetsel et al., 2014). In the last decade, there have warmth, hostility, and anxious behavior between
been increased efforts to include fathers in these anxious mothers and fathers during the interac-
studies, as previously very little was known about tion task.
the role they play in the development of child Another study examining the parenting behav-
anxiety disorders. Interestingly, one meta- iors of anxious parents of 10- to 15-month-old
analysis found that the association between par- infants found that fathers with social anxiety dis-
enting behaviors and child anxiety symptoms order reported more overinvolvement and less
was stronger for fathers than mothers (Moller challenging parent behavior (i.e., behavior that
et al., 2016). In contrast, a previous meta-analysis encourages the child to go outside his/her com-
by McLeod et al. (2007) found that parent’s gen- fort zone (Moller et al., 2015)). Others have
der did not moderate the relationship between found that fathers’ (but not mothers’) PTSD
parenting and child anxiety symptoms. symptoms predicted whether their children
Research suggests that fathers of anxious chil- developed PTSD following a natural disaster
dren demonstrate more controlling and less help- (Kilic et al., 2003). In another study, paternal
ful behavior toward their children (Bogels & somatization negatively predicted children’s self-
Phares, 2008). Additional studies have focused reported anxiety symptoms following treatment
(Crawford & Manassis, 2001). Taken together, he Role of Parenting in Specific

T
this evidence suggests that anxious fathers may Anxiety Disorders
engage in behaviors which could impact child
anxiety development. Social Anxiety Disorder
Parental expressions of anxiety as well as
encouragement have also been examined for In the last decade, research has increasingly
mothers and fathers. In a study by Moller and examined parenting influences on the develop-
colleagues (2014), 10- to 15-month-old infants ment of specific anxiety disorders in children and
were randomly assigned to complete the visual adolescents. A variety of studies have examined
cliff task with either their mother or their father. parenting and social anxiety disorder in youth,
Results indicated that expressed anxiety from with results highlighting a number of potentially
fathers, but not mothers, was related to increased relevant parenting factors. For example, there is
expressions of anxiety and avoidance for infants. evidence that parents of socially anxious children
Of note, this association was moderated by infant demonstrate more overinvolvement and control-
anxious temperament; specifically, fathers’ ling behaviors during tasks with their child
expressed anxiety was more strongly associated (Asbrand et al., 2017; Greco & Morris, 2002).
with infant avoidance and anxiety when infants Mothers of children with more social anxiety
were temperamentally anxious. symptoms were less flexible and less responsive
There has also been interest in looking at the to their child’s needs during a puzzle task than
transactional relationship between parents in mothers of healthy control children, whose
relation to the development of child anxiety. To behavior was more responsive to their child’s
do this, one study utilized the actor-partner inter- needs (e.g., increasing maternal involvement in
dependence model, which takes into account the the task if the child requested it (Asbrand et al.,
notion that parents’ relationships with one 2017)). Another study found that the specific
another are interdependent and transactional, combination of maternal overprotection, paternal
with each parents’ anxiety influencing not only rejection, and paternal lower emotional warmth
their own parenting behaviors but also the parent- was uniquely related to social phobia among ado-
ing behaviors of their partner (Gibler et al., 2018). lescents (Knappe et al., 2012). Further, among
Parents completed self-report measures of anxi- parents with social anxiety disorder, parenting
ety and parenting behaviors, and their 12- to behaviors including overcontrol, low levels of
30-month-old infant participated in a laboratory warmth, and transfer of threat information via
task assessing anxiety risk. Results indicated that parental modeling are more common, and these
although there was no direct association between behavioral tendencies are theorized to increase
parent anxiety and child anxiety, paternal anxiety child social anxiety symptoms by reducing
was indirectly associated with child anxiety risk opportunities to learn and practice effective social
via its influence on maternal encouragement of skills, increasing child avoidance of social situa-
independence. Specifically, paternal anxiety was tions, and reducing children’s self-efficacy
associated with decreased maternal encourage- (Garcia et al., 2021).
ment of independence, which in turn was related Some studies have examined moderators and
to child anxiety risk. mediators of the relationship between parenting
In recent years, the increasing inclusion of and social anxiety symptoms in children. In a
fathers in child anxiety research has empirically study involving 9- to 12-year-olds who com-
highlighted the important role that fathers play in pleted an origami task with both of their parents,
the development of child anxiety symptoms. Morris and Oosterhoff (2016) found that
Although results to date are somewhat mixed, it increased maternal verbal instruction during the
is clear that continued investigation of fathers’ task was associated with lower levels of child
roles, as well as further examination of potential social anxiety symptoms. In contrast, increased
mediators and moderators, is warranted. paternal verbal instruction was associated with
higher social anxiety for male children and lower well as a number of moderators and mediators
social anxiety for female children. This study which warrant further examination.
also found that children with higher levels of
social anxiety symptoms had fathers who made
more critical statements and mothers who more Generalized Anxiety Disorder
frequently physically took over the task. Another
study found an indirect effect of psychological A number of studies have also examined parent-
control on child social anxiety; specifically, ing practices in relation to generalized anxiety
among mothers (but not fathers), higher anxiety disorder (GAD) and/or worry among children.
about their daughters’ well-being was associated Parenting practices that have been found to be
with more use of psychological control, which in related to increased levels of worry in children
turn was related to higher levels of child social and adolescents include increased levels of rejec-
anxiety symptoms (Bynion et al., 2017). In addition (Brown & Whiteside, 2008; Hale et al.,
tion, Gomez-Ortiz and colleagues (2019) found 2006; Muris et al., 2000), anxious rearing behav-
that parenting practices including low levels of iors (Muris, 2002; Muris et al., 2000), parental
affection and communication, humor, reduced control (Muris, 2002), and parental alienation
autonomy promotion, and increased psychologi- (Hale et al., 2006). With respect to GAD specifi-
cal control predicted negative self-esteem among cally, Muris and Merckelbach (1998) found that
children, which predicted social anxiety among 8- to 12-year-old children, both parental
symptoms. control and anxious child-rearing practices were
Studies utilizing experimental designs have associated with GAD symptoms. Similar results
increasingly been conducted. One study pre- were found by Morris and Oosterhoff (2016),
sented a community sample of 8- to 12-year-old who found that observed measures of parental
Dutch children with vignettes depicting ambigu- rejection (i.e., denying reassurance) and control
ous social situations in which the parent (i.e., physical takeovers during an origami task)
responded either anxiously or confidently (Bogels were associated with increased levels of GAD
et al., 2011). Children were then asked to rate symptoms among children. In contrast, Wilson
their level of social anxiety versus confidence in et al. (2011) found no significant associations
the fictional situation. Results indicated that between self- and child-reported parenting
among more socially anxious children, the behavior and child worry.
father’s response in the vignette influenced the There is much discussion about the direction
children’s level of confidence more than the of effects between children and parents when it
mother’s vignette response. This finding was not comes to the development of anxiety symptoms.
consistent among subclinical youth. Among chil- One study attempted to examine this and found
dren with no or low levels of social anxiety, the evidence supporting the notion that children
mother’s response in the vignette relative to the evoke different parenting practices depending on
father’s response influenced the child’s response the level of anxiety they experience (Wijsbroek
more. In another study, researchers manipulated et al., 2011). Specifically, this study found that
infants’ mothers’ response style (i.e., confident or adolescents with high levels of self-reported
socially anxious) when interacting with a stranger GAD and separation anxiety disorder symptoms
(de Rosnay et al., 2006). Results indicated that at the first time point reported increases in paren-
behaviorally inhibited infants responded with tal control over time.
more socially anxious behavior toward the Overall, the literature to date examining par-
stranger when their mother also demonstrated enting practices and their relation to GAD in
socially anxious behavior toward the stranger. youth has highlighted many of the same parent-
Overall, the literature on parenting influences ing practices which have been implicated in the
and social anxiety disorder in children has high- development of other anxiety disorders, as well
lighted several important parenting behaviors, as as anxiety symptoms more generally.
Challenging Parenting Behavior intentional teasing. Results indicated that moth-

ers’ and fathers’ encouragement of social asser-
Challenging parenting behavior represents a relation and engagement in new situations was
tively new construct within the parenting and associated with lower levels of social anxiety
anxiety literature. This construct builds upon symptoms in early adulthood. Further, higher
theoretical work related to the potentially differ- levels of paternal intentional teasing predicted
ing roles that mothers and fathers may play in higher levels of adult social anxiety symptoms.
parenting. Paquette (2004) postulated that fathers Another study examined CPB in emerging adult-
“seem to have a tendency to surprise children, to hood (i.e., ages 18–25) and found that higher
destabilize them momentarily, and to encourage paternal social CPB was associated with lower
them take ‘risks,’ thus enabling children to learn levels of social anxiety symptoms (Smout et al.,
to be brave in unfamiliar situations and to stand 2020).
up for themselves” (p. 212). Challenging parent- CPB has been examined in early childhood as
ing behavior (CPB) is defined as parenting well as emerging adulthood and has some early
behavior that “promotes assertiveness, taking support as a potential protective parenting factor
chances, and overcoming limits” (Majdandzic when it comes to the development of child and
et al., 2016, pp. 424), with examples of CPB adolescent anxiety. Aspects of CPB, including
including rough and tumble play, tickling, and encouragement of social assertion and encour-
encouraging the child to push their limits physi- agement to engage in new situations, may serve
cally or socio-emotionally. to reduce youth avoidance of anxiety-provoking
Several studies have examined the relation- situations, which would theoretically buffer
ship between CPB and childhood anxiety, finding against the development or maintenance of anxi-
some evidence for a relationship between mater- ety symptoms. Given findings to date, additional
nal and paternal CPB and lower levels of anxiety research focused on CPB may provide further
in preschool-aged children (Lazarus et al., 2016; insight into how to protect against the develop-
Majdandzic et al., 2018b). Another study found ment of anxiety symptoms in youth.
that among preschool-aged children, having at
least one parent with high CPB predicted fewer
anxiety symptoms, even when the co-parent arenting and Childhood Anxiety
P
demonstrated lower levels of CPB (Majdandzic Prevention and Intervention
et al., 2018a). However, Majdandzic and col-
leagues (2014) found a difference in the relation- Intervention and prevention studies can also shed
ship between mothers’ and fathers’ CPB and light on parenting factors that impact the devel-
child social anxiety symptoms, with fathers’ CPB opment and maintenance of child anxiety. In par-
negatively predicting observed social anxiety ticular, some studies have explicitly targeted
symptoms in their 4-year-old children and moth- parenting practices as a means of reducing child
ers’ CPB predicting higher observed social anxi- anxiety symptoms, while others have measured
ety symptoms in their child. parenting practices to determine whether treat-
One study has examined CPB retrospectively ment has had an impact on these. Although a full
in a sample of undergraduate college students. exploration of child anxiety prevention and inter-
Undergraduates completed a retrospective mea- vention literature is beyond the scope of this
sure of their perception of their parents’ CPB chapter, the following section discusses this lit-
from ages 7 to 12, as well as a measure of current erature as it pertains to parenting behaviors.
social anxiety symptoms (Lazarus et al., 2018). Many studies have examined whether parental
An exploratory factor analysis identified three involvement in CBT for youth anxiety disorders
constructs comprising CPB, including parental yields additional benefit beyond child-focused
encouragement of social assertion, parental treatments alone, with mixed results overall.
encouragement to engage in new situations, and Some studies have suggested that there is no
significant benefit to including parents in treat- particularly when treatment specifically helps
ment compared to child-focused CBT (Breinholst parents reduce children’s avoidance of anxiety-
et al., 2012; Peris et al., 2021; Thulin et al., 2014), provoking stimuli.
while others have found that parent’s involve- Similarly, in acknowledging that parental
ment is associated with improved outcomes involvement in youth CBT for anxiety can be
(Manassis et al., 2014; Sun et al., 2018). defined in a number of ways, a meta-analysis by
Silverman et al. (2021) shed additional light on Manassis et al. (2014) sought to compare child
this issue. In this study, families with a child anxiety outcomes across three groups: child-
meeting criteria for an anxiety disorder were ran- focused CBT with limited parental involvement,
domly assigned to one of three treatment groups: CBT with family involvement focused on contin-
individual child CBT, CBT with parent’s involve- gency management (CM) or transfer of control
ment focused on reinforcement training (i.e., (TC) from therapist to parent, and CBT with fam-
teaching parents to not allow their child to avoid ily involvement with low emphasis on CM or TC.
anxiety-provoking situations, CBT + reinforce- Results indicated that while all three forms of
ment), or CBT with parent involvement focused treatment led to reductions in child anxiety symp-
on improving the parent-child relationship (i.e., toms, those who received CBT with family
improving acceptance and reducing psychologi- involvement with a strong emphasis on CM and/
cal control, CBT + relationship). Parents ran- or TC continued to experience increased rates of
domized to the CBT + reinforcement treatment anxiety disorder remission during the period of
had lower self-reported ratings of negative rein- time between post-treatment and 1-year follow-
forcement (i.e., allowing their child to avoid up, compared with children in the other two inter-
anxiety- provoking situations) at post-treatment vention groups, whose gains were simply
compared to parents in the CBT + relationship or maintained. These results further demonstrate
child-focused CBT conditions, suggesting treat- that more clearly defining the specific focus of
ment specificity. In other words, simply involv- parent-based components of CBT for child anxi-
ing the parent in treatment did not significantly ety is important when attempting to evaluate
reduce negative reinforcement; rather, this was whether parent involvement yields additional
only found when the parent-focused treatment benefit beyond child-focused CBT alone.
specifically targeted this component. At post- Others have attempted to investigate the direc-
treatment, results indicated no significant differ- tion of effects between children and parents or
ence between the three treatment conditions how parents and children may impact change in
based on parent’s report of child anxiety; how- one another as a result of treatment. One study by
ever, children randomized to one of the two Settipani et al. (2013) assessed child anxiety
parent-focused treatment conditions had lower symptoms as well as parent variables, including
self-reported anxiety scores at post-treatment. In maternal anxiety, maternal psychological con-
addition, at the 12-month follow-up, parent’s trol, family affective involvement, and family
reports of child anxiety symptoms were signifi- behavioral control among children ages 7–14
cantly lower for children in the CBT + relation- who completed CBT treatment for anxiety.
ship condition. Further, lower levels of parent’s Results suggested that decreases in child anxiety,
negative reinforcement at post-treatment were as rated by mothers, led to decreases in maternal
significantly associated with lower levels of anxiety. In addition, decreases in maternal psy-
parent-reported child anxiety symptoms. Lastly, chological control and family affective involve-
reductions in parents’ negative reinforcement ment from pre- to post-treatment preceded
were associated with reductions in parents’ use decreases in clinician-rated child anxiety from
of psychological control, which partially medi- the post-treatment to follow-up period. Taken
ated anxiety reduction. Overall, conclusions from together, results suggest a bidirectional influence
this study suggest that parent involvement in between parents and children during the treat-
treatment for child anxiety disorders is beneficial, ment process.
In addition to the treatment literature, the lit- gested that baseline child anxiety symptoms
erature regarding prevention programs for youth moderated CAPS treatment effects, with children
anxiety disorders has provided insight into the with higher levels of anxiety benefitting more
role parenting behaviors may play in the develop- from the intervention than those with lower base-
ment of child anxiety disorders. In particular, a line anxiety levels. Further, parental anxious
program developed by Ginsburg (2009) has modeling and global parental distress mediated
shown promise in preventing the development of effects on outcomes among children who received
child anxiety disorders in children of anxious CAPS. Specifically, CAPS led to reductions in
parents. The program, Coping and Promoting parental anxious modeling and global parent dis-
Strength (CAPS) Program, specifically targets tress, which led to reduced anxiety symptoms
malleable anxiety risk factors in children (i.e., among youth. Notably, results suggested that
anxiety symptoms, maladaptive cognitions, and both child maladaptive cognitions and parent
poor coping/problem-solving skills) and parents anxiety did not serve as moderators of treatment
(anxious modeling, anxiety-enhancing parenting outcome. Given these results, the authors argue
practices such as overcontrol, and criticism/family that interventions and/or prevention programs
conflict). The program is delivered across 6–8 targeting parent anxious modeling as well as par-
weekly sessions and includes parents alone for ent distress may be beneficial in preventing the
the first two sessions, though any family member development of anxiety disorders in children.
can join for the remaining sessions. Interventions Taken together, the results of recent preven-
include CBT strategies targeting anxiety, cognition and intervention studies addressing the link
tive restructuring, building communication and between parenting behaviors and child anxiety
problem-solving skills, and contingency manage- disorders suggest several areas of potential prom-
ment. Participants in the pilot study, which com- ise. Although the larger literature base has mixed
pared CAPS to a wait-list control group, included results in terms of whether parent involvement in
40 nonanxious children, ages 7–12, and their CBT for youth anxiety improves outcomes
family, where one parent met criteria for an anxi- beyond those gained from child-focused CBT,
ety disorder. Results indicated that 30% of the recent literature suggests that when interventions
children in the wait-list control group developed specifically target parenting practices associated
an anxiety disorder by the 1-year follow-up with child anxiety development, results are more
assessment, while none of the 20 children who promising. Specifically, parent-focused interven-
received CAPS developed an anxiety disorder tions targeting improving contingency manage-
(2009). ment, reducing parent psychological control, and
Ginsburg et al. (2015) later conducted a ran- reducing anxious parental modeling may increase
domized controlled trial comparing CAPS to an effectiveness of CBT treatment for youth
information-monitoring control condition, in anxiety.
which families received a pamphlet about anxiety
disorders and treatment. Participants included
nonanxious children, ages 6–13, from families in Summary and Future Directions
which one parent had an anxiety disorder diagno-
sis. Results indicated that across the 1-year study The field of child anxiety and parenting is cur-
period, rates of anxiety disorder diagnosis were rently making exciting progress. We have
5% in the CAPS condition and 31% in the expanded our understanding of the specificity of
information- monitoring control condition. In traditional theoretical models, such as maternal
addition, children who received CAPS both had anxiety as a risk factor for child anxiety, and
significantly lower anxiety scores at the post- increased our understanding of new risk factors
treatment assessment, as well as at the 6- and and influences, such as fathers’ role in childhood
12-month follow-up time points, compared to the anxiety disorders.
control group. Interestingly, results also sug-
Although many questions remain, recent psychological control affects children and adolescents
(pp. 15–52). American Psychological Association.
research in this area continues to point toward Barber, B. K., Xia, M., Olsen, J. A., McNeely, C. A.,
parenting practices as a key research focus. The & Bose, K. (2012). Feeling disrespected by parents:
parenting and anxiety literature will benefit from Refining the measurement and understanding of
studies which increase the breadth of experimen- psychological control. Journal of Adolescence, 35,
273–287.
tal and intervention designs including parents, Bates, J. E. (1980). The concept of difficult tempera-
particularly fathers, who have been understudied ment. Merrill-Palmer Quarterly of Behavior and
in the current literature. As with the majority of Development, 26(4), 299–319.
studies in the field of psychology, recent studies Bayer, J. K., Morgan, A., Prendergast, L. A., Beatson, R.,
Gilbertson, T., Bretherton, L., Hiscock, H., & Rapee,
would benefit from replication in naturalistic R. M. (2019). Predicting temperamentally inhibited
study settings. Additionally, future studies should young children’s clinical-level anxiety and internal-
work to further increase our understanding of izing problems from parenting and parent wellbe-
moderators and mediators impacting the relation- ing: A population study. Journal of Abnormal Child
Psychology, 47(7), 1165–1181.
ship between parenting and child anxiety Beidel, D. C., & Turner, S. M. (1997). At risk for anxi-
development. ety: Psychopathology in the offspring of anxious par-
Another focus of the literature moving for- ents. Journal of the American Academy of Child and
ward should be directionality of change, namely, Adolescent Psychiatry, 36, 918–924.
Bögels, S., & Phares, V. (2008). Fathers’ role in the eti-
the possibility that heightened child anxiety ology, prevention and treatment of child anxiety: A
states may actually elicit parental overcontrol and review and new model. Clinical Psychology Review,
anxious behavioral modeling. The reciprocal 28(4), 539–558.
influence of child and parental traits has become Bögels, S. M., van Oosten, A., Muris, P., & Smulders,
P. (2001). Familial correlates of social anxiety in
part of the standard child anxiety model (e.g., children and adolescents. Behaviour Research and
Rapee (2001)); however, few experimental Therapy, 39, 273–287.
designs have tested the reciprocal nature of such Bögels, S., Stevens, J., & Majdandžić, M. (2011).
traits. Such focus on these traits will continue to Parenting and social anxiety: Fathers’ versus moth-
ers’ influence on their children’s anxiety in ambigu-
inform childhood anxiety interventions, increas- ous social situations. Journal of Child Psychology and
ing the efficacy of our current gold standard Psychiatry, 52(5), 599–606.
treatments. Biederman, J., Newcorn, J., & Sprich, S. (1991).
Comorbidity of attention deficit hyperactivity disorder
with conduct, depressive, anxiety, and other disorders.
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Part III
Specific Phobias in Children
and Adolescents 16
Thompson E. Davis III, Jerrica Guidry,
and Thomas H. Ollendick
Introduction (e.g., dogs or bees) while later gains in abstract

and social thought lead to more abstract and
Specific phobias (SD) are intense fears of certain intangible fears (e.g., the “boogeyman” or public
objects, animals, situations, or environments. embarrassment; Davis (2009), Gullone (2000)
While not as severe as other more pervasive anxi- and Muris et al. (2002)). For example, animal
ety disorders (e.g., generalized anxiety disorder, fears have an onset around 7 years of age, fol-
obsessive-compulsive disorder), a specific pho- lowed by increasingly abstract situational and
bia can be a serious impediment to a child’s suc- social fears in the teenage years (Davis et al.,
cessful development and can carry significant 2009a; Öst, 1987a). While these fears typically
long-term psychological and social effects, usu- arise and subside, presumably alleviated by
ally into adulthood (Davis, 2009; Davis et al., increased instruction and exposure to the feared
2009b). Even so, fear itself is important, normal, stimulus, not all childhood fears are just a “phase”
and highly adaptive (Davis, 2009). The experi- or transitory in nature (Ollendick et al., 2009a).
ence of fear often is healthy and keeps us safe
(e.g., looking both ways before crossing the street
and exercising caution around strange dogs). The Phenomenology
emergence of fear roughly coincides with increas-
ing cognitive-developmental gains and is a sign Some seemingly developmentally appropriate
of cognitive maturation. Early concrete thinking fears persist despite the best efforts of parents,
is associated with fears of highly specific stimuli other caregivers, and family doctors, and are
unusually frequent, intense, and distressing, lead-
ing to a disruption of the child’s life. In order to
Author Notes: The terms “child” and “children” are used
throughout and usually meant to include adolescents be diagnosed with this kind of problematic and
unless otherwise noted. persistent fear, a child must have the fear for at
T. E. DavisIII (*) · J. Guidry

Department of Psychology, Louisiana State
University,
Baton Rouge, LA, USA
e-mail: ted@lsu.edu
T. H. Ollendick
Virginia Tech, Blacksburg, VA, USA
https://doi.org/10.1007/978-3-031-14080-8_16
236 T. E. Davis et al.
least 6 months with accompanying problematic cians must plan for treatment generalization to
avoidance or distress (i.e., interference), along combat the spontaneous recovery of fear (Bouton,
with physiological symptoms (APA, 2013). Such 2004).
symptoms are said to constitute a “specific pho- Several developmental adaptations to the typi-
bia” that can be further classified into one of sev- cal diagnostic criteria must also be considered.
eral types: animal (i.e., both animals and insects), Children may not be able to fully articulate their
natural environment (e.g., the dark or heights), fears or cognitions and may not realize their fear
blood-injection-injury (e.g., receiving an injec- or their response when exposed is extreme (Davis
tion or seeing blood), situational (e.g., small et al., 2009b; APA, 2013). A child may also
enclosed spaces or flying in an airplane), or other become clingy, cry, or possibly even become
(e.g., loud noises, clowns, costumed characters, aggressive when exposure is forced or escape
vomit, and fears that do not fit the previous types; prevented (APA, 2013; Davis & Ollendick,
APA, 2013). 2014). Finally and as noted above, to avoid mis-
Those having a specific phobia are thought to diagnosing the typical developmental progres-
experience an unusually strong, pathological sion of fears as clinically significant specific
emotional response of a neural fear network of phobias, a child must also have the fear for at
memories and prepotent responses (Davis & least 6 months.
Ollendick, 2005; Lang, 1979; Note: this is differ- Unfortunately, relatively little research has
ent than neural circuitry—for a review see Chap. focused on the phenomenology of specific pho-
5). From this information-processing model, a bias in children and adolescents. From what is
specific phobia is a psychopathological combina- known, it appears that specific phobias affect
tion of physiology, behavior, and cognition. With children from a variety of racial, ethnic, and
exposure to cues associated with the feared stim- socioeconomic backgrounds (Oar et al., 2019;
ulus, children with specific phobias typically Ollendick et al., 2010). Also, it appears that ani-
experience activation of the autonomic nervous mal and natural environment type specific pho-
system (e.g., increased heart rate), usually bias are the most common (Last et al., 1992;
attempt to engage in avoidance behavior (e.g., Milne et al., 1995; Ollendick et al., 2009b, 2010;
running away), and think catastrophic thoughts Silverman et al., 1999), with phobias of dogs,
(e.g., “the dog is going to bite me,” “the lightning insects, heights, the dark, and storms being
will strike our house and burn it down”; Davis common. Children with specific phobias differ
and Ollendick (2005)). When all three compo- by type too. Ollendick et al. (2010) found that
nents of the emotional response appear, synchro- children with natural environment phobias were
nous responding occurs; however, desynchronous more impaired than those with animal phobias in
or partial responses can occur as well (i.e., their somatic and anxious symptoms, depressive
incomplete or partial activation of the fear net- symptoms, and life satisfaction (i.e., a measure
work resulting in a partial response or only a of quality of life). Moreover, on the Child
response in one or two components; Hodgson Behavior Checklist (Achenbach, 1991), they
and Rachman (1974), Rachman and Hodgson were rated as being more withdrawn, having
(1974)). Given this, a clinician’s treatment goal is more somatic complaints, being more anxious/
to alter this fear network of memories and depressed, and having more social problems
responses (e.g., learning histories, conditioning than children with animal phobias. Even so, no
experiences, stimulus characteristics) and differences emerged between the two groups of
through therapy create new, adaptive, memories children on socioeconomic variables, demo-
which will compete with the previous psycho- graphic variables, family variables, severity of
pathological information (Bouton, 2004; Davis, the specific phobias themselves, or ratings of
2009). This type of corrective learning experi- coping or dangerousness of their feared stimuli
ence also tends to be context specific so clini- (Ollendick et al., 2010).
16 Specific Phobias in Children and Adolescents 237
Comorbidity also appears to be the rule for Epidemiology

children with specific phobias in both commu-
nity and clinical samples. Comorbidity rates Overall, anxiety disorders are the most com-
tend to vary greatly, however, with approxi- monly occurring group of psychological disor-
mately half of all children with specific phobias ders, and of the anxiety disorders, specific phobia
having another comorbid specific phobia in is the most prevalent with a 12-month prevalence
community samples (25% may have another rate of 8.7% and a lifetime prevalence rate of
disorder; Costello et al. (2004)). This rate is 12.5% (Kessler et al., 2005a, b). In children,
comparable to clinical samples, although the approximately 5% of community samples and
rates vary considerably. For example, Öst et al. 10% of clinical samples have fears persistent and
(2001) found 42% of children were comorbid intense enough to be deemed specific phobias
with at least one other disorder, Last et al. (APA, 2013; Ollendick et al., 1997). Higher rates
(1992) found 50% were comorbid, Silverman have been reported, however, with some studies
et al. (1999) found 72% were comorbid, and suggesting 17.6% of parent-reported childhood
Ollendick et al. (2009b) found 95% of their fears are severe enough to be specific phobias
sample were comorbid—half with at least (Muris & Merckelbach, 2000) and 22.8% of
another specific phobia. Comorbidity appears child-reported fears may be phobic disorders
to be characterized by other specific phobias or (Muris et al., 2000). Further, among adolescents,
other anxiety disorders; however, other comor- lifetime prevalence has been found to be 19.3%
bid internalizing and externalizing disorders (Merikangas et al., 2010). In addition, while the
have been observed as well (e.g., attention-def- mean age of onset has been suggested to be
icit/hyperactivity disorder and oppositional 9–10 years (Stinson et al., 2007), there is wide
defiant disorder; Ollendick et al., 2010). variability depending on the type of fear, ranging
Overall, the most common comorbid diagnoses in emergence from early childhood to early adult-
appear to be other specific phobias, and then, in hood (Öst, 1987a). Unfortunately, the toll exacted
varying order depending on the study, general- by specific phobia on the health-care system and
ized anxiety disorder, social phobia, separation those with the fear has been great with those hav-
anxiety disorder, attention-deficit/hyperactivity ing specific phobias accessing medical care at
disorder, and major depression (Ollendick higher rates than those with obsessive-compulsive
et al., 2009b, 2010; Öst et al., 2001). To date, disorder, and second only to panic disorder
only one study has reported on comorbidity dif- (Deacon et al., 2008). Specific phobias are also
ferences by type of specific phobia: Ollendick associated with poor outcomes of internalizing
et al. (2010) found higher rates of generalized disorders and severe mental disorders throughout
anxiety disorder and separation anxiety disor- a person’s life span (de Vries et al., 2019). Even
der in children having a natural environment so, fewer than 10% of adults ever seek treatment
type phobia compared to an animal type pho- for specific phobia, and most have had their fear
bia. Comorbidity with other more severe disor- for an average of 20 years, presumably because
ders is also common (e.g., autism spectrum of the degree of accommodation in daily life and
disorder; Davis et al. (2014)). Practitioners overall avoidance (Stinson et al., 2007).
should be slow and cautious when applying Additionally, fewer than 30% of youth receive
assessment and therapy techniques developed treatment for specific phobia (Ollendick et al.,
for typically developing children with those 2018). The lack of treatment-seeking is even
who may be atypically developing (e.g., autism more concerning when the evidence for quick,
spectrum disorder) without modifications or efficacious outcomes related to the treatment of
proper training (Davis, 2013; Davis et al., 2014; specific phobia is considered (see Davis and
Hagopian et al., 2017; Moree & Davis, 2010; Ollendick (2005), Davis et al. (2011), and Öst
Muskett et al., 2019). and Ollendick (2017)).
Etiology studies specifically focused on youth and aspects

of anxiety and fear may provide a richer under-
The exact causes of specific phobias are still not standing. For example, understanding the rela-
well understood; likely there are myriad causes tionships between structures of the brain and
that act alone or in combination to bring about a symptoms such as anxious arousal and anxious
specific phobia depending on the characteristics apprehension in youth may begin to move our
of the individual (Davis, 2009). Four common understanding further (Castagna et al., 2018).
pathways are recognized, however, and grouped
into three associative accounts (classical condi-
tioning, modeling, and transmission of negative Evidence-Based Assessment
information) and one other pathway (the nonas-
sociative account; Nebel-Schwam and Davis With the rise of evidence-based practice, and
(2013), Poulton and Menzies (2002), Rachman empirically supported treatments in particular, a
(1977, 2002)). Classically conditioned phobias detailed and thorough assessment prior to com-
are acquired through direct contact with the stim- mencing treatment has become essential to the
ulus (e.g., a snake bites a child). Phobias acquired provision of clinical services. While a thorough
through modeling involve seeing another indi- description of the assessment process is beyond
vidual behave afraid (e.g., a parent acts very the scope of this chapter (see Ollendick et al.
afraid of snakes in front of the child). The trans- (2004), Silverman and Ollendick (2005), and
mission of negative information serves to impart Etkin et al. (2021) for reviews), a clinician choos-
fear through the retelling of scary stories, cata- ing an evidence-based treatment should carefully
strophic beliefs about the stimulus, and the like consider the assessments used in the studies upon
(e.g., a parent tells a child to only play inside which the evidence has been built so an accurate
their yard because snakes are everywhere and and compatible diagnosis can be made (i.e., using
will bite you). Finally, the nonassociative account the same assessment techniques as the evidence
attempts to capture those fears that seem to have to know if a patient does have a disorder similar
more of a biological or genetic predisposition to that in a particular randomized trial and there-
(Rachman, 2002), though often individuals who fore possibly amenable to that treatment). In
have difficulty in recalling the exact origin of addition, a comprehensive assessment should
their fear are relegated to this category (e.g., “I allow for a detailed diagnostic assessment of
don’t know; I’ve always been afraid of snakes”). childhood disorders (including comorbid
Even so, additional consideration is necessary as conditions) and it should include direct examina-
many individuals experience associative events tion of the phobic response (i.e., psychophysiol-
and do not develop a specific phobia (e.g., many ogy, behavior, and cognition; Davis and Ollendick
people have been bitten by dogs but do not (2005), Ollendick et al. (2009a)). The assessment
develop a phobia). While any one path may cause should be multi-method and multi-informant: use
a specific phobia, it is likely that associative of a variety of techniques and respondents to be
experiences increase over time until interacting sure an accurate diagnostic picture emerges
with an individual’s own unique nonassociative across different situations. Instruments and inter-
vulnerability (Nebel-Schwalm & Davis, 2013; views typically recommended for this type of
Ollendick & King, 1991; Ollendick et al., 2002). assessment include the Anxiety Disorders
As a result, the answer may be summarized as it Interview Schedule for DSM-IV Child/Parent
is simply a matter of determining how much version (ADIS-IV-C/P; diagnostic interview;
associative experience is necessary for an indi- Silverman and Albano (1996), and its DSM-5
vidual to develop a specific phobia given his or revision, Albano and Silverman (in press)), the
her unique inborn diatheses and competing cor- Multidimensional Anxiety Scale for Children
rective experiences (Marks, 2002). Additionally, 2nd Edition (MASC-2; anxiety self-report mea-
the increased use of imaging techniques and sure; March (2013)), the Fear Survey Schedule
for Children-Revised (FSSC-R; fear self-report treatments for child specific phobia, an emphasis
measure; Ollendick (1983)), and the Child will be placed on the newer, empirically sup-
Behavior Checklist (CBCL; broadband parent- ported, intensive CBT called “One-Session
report measure; Achenbach (1991)), among oth- Treatment” (OST; Davis et al., 2012b, 2019; Öst,
ers. Phobia-specific questionnaires can be 1987b, 1989; Ollendick et al., 2009b; Zlomke &
considered for inclusion as well (e.g., question- Davis, 2008). Currently, there are four major
naires about particular stimuli like spiders). types of empirically supported treatment for
Behavioral avoidance tasks (BATs) should be child specific phobia: systematic desensitization,
considered for inclusion by clinicians because of reinforced practice (also called contingency man-
the unique psychophysiological, behavioral, and agement), modeling and participant modeling,
cognitive information they can offer (Castagna and CBT (Davis, 2009; Davis et al., 2011; Davis
et al., 2017; Davis et al., 2009b, 2012b, 2013; & Ollendick, 2005; Seligman & Ollendick,
Ollendick et al., 2009a), as well as family interac- 2012). Given this, it is no surprise then that the
tion characteristics (Ollendick et al., 2012). most widely used treatment components for chil-
While these behavioral avoidance tasks may be dren with anxiety have been exposure, relaxation,
difficult to arrange (e.g., getting, storing, and car- cognitive restructuring, modeling, psychoeduca-
ing for stimuli or arranging for offsite visits), tion, and reinforcement (Chorpita & Daleiden,
especially for private practitioners with limited 2009; Farrell et al., 2019).
resources, help, and space, the incorporation of
BATs into the assessment process has been
strongly encouraged as it provides valuable infor- Systematic Desensitization (SD)
mation about how the child will respond during
an actual encounter with the stimulus or situation Systematic desensitization is one of the earliest
(Davis et al., 2009b). Ideally, a comprehensive and most influential child treatments for specific
pretreatment assessment will provide enough phobia, though its underlying theory and use
information to determine a diagnosis of specific have been increasingly challenged and criticized
phobia, identify any comorbid diagnoses which (Davis, 2009; Ollendick et al., 2009a). According
may require additional treatment or need to be to Wolpe (1958), SD works through a process of
considered during treatment for the phobia (e.g., reciprocal inhibition—the notion that one cannot
separation anxiety disorder in addition to a specific experience two competing emotions simultane-
phobia of the dark), and plan the steps of a grad- ously. The goal is to work toward extinguishing
ual, hierarchical exposure (typically in vivo). the classically conditioned fear response by
weakening the ability of the conditioned stimulus
to elicit the conditioned response (e.g., a dog no
Treatment longer elicits a fear response). A necessary com-
ponent, then, becomes exposure to the feared
Empirically Supported Treatments stimulus while an emotion other than fear is
experienced. Typically, the exposure in this
Currently, clinicians seeking to treat child and approach has been imaginal, not in vivo. This is
adolescent fears have a variety of well-researched accomplished by carefully constructing a gradu-
techniques available in their clinical armamen- ated imaginal fear hierarchy with the child’s
tarium. These options have come from decades of input and then inducing an incompatible emotion
study leading to the identification of several treat- in the child during each step of the exposure.
ments for child anxiety and fear (e.g., applied Wolpe (1958) recommends any appetitive behav-
behavior analyses [ABA], behavior therapy [BT], ior—for example, humor or eating—but progres-
and cognitive-behavioral therapy [CBT]). sive muscle relaxation (PMR) has come to be the
Following a brief review of the established primary technique of choice. Treatment pro-
gresses by initially developing the graduated fear Modeling and Participant

hierarchy and then instructing the child in PMR Modeling (PM)
until mastery is achieved. Several scripts for
PMR exist (e.g., see Ollendick and Cerny (1981)), Modeling is based on social learning theory with
but they all involve training the child to progress treatment progressing by having a model (usually
through various muscle groups by briefly tensing the clinician) demonstrate the successful comple-
and relaxing them (Ollendick et al., 2004). tion of steps in the fear hierarchy to the child
Importantly, for this treatment to be effective, the (Davis & Ollendick, 2005). Originally called
child should not actually experience high levels contact desensitization (Ritter, 1965, 1968), par-
of fear, but rather the associative strength of the ticipant modeling carries this procedure further
conditioned stimulus and response should be by actually incorporating the child into the expo-
weakened by not feeling afraid during exposure sure by having the clinician successfully model
(Davis, 2009; Davis & Ollendick, 2005). While the completion of a particular step in the fear
initially it was one of the treatments of choice for hierarchy and then involve the child in complet-
specific phobia, enthusiasm for SD in research ing the modeled step (Davis, 2009; Davis &
has waned over the past several decades as the Ollendick, 2005; Ollendick et al., 2009a). The
field has moved toward fewer distractions from child can be incorporated using a number of tech-
exposure (e.g., relaxation training). niques depending upon the child’s ability to
negotiate the steps: the clinician may simply pro-
vide verbal instruction on the completion of the
Reinforced Practice (RP) step or may go as far as to engage in physical
contact ranging from simply standing beside the
Based upon operant conditioning and ABA prin- child while holding hands to using hand-over-
ciples, a clinician using RP attempts to reinforce hand assistance in close proximity to the feared
successive steps toward feared stimuli, thereby stimulus to help the child voluntarily complete
overcoming avoidance behavior (Davis & the step (i.e., as opposed to compulsory hand-
Ollendick, 2005). Reinforced practice requires over-hand procedures seen in three-step prompt-
the clinician to again devise a detailed fear hier- ing; Miltenberger (2001)).
archy, but also to conduct a functional assess-
ment to determine the maintaining functions of
the avoidance (including any secondary gains) Cognitive-Behavioral Therapy (CBT)
and a reinforcer survey to create an array of
reinforcers to apply contingently upon comple- Cognitive-behavioral therapy is a combination
tion of the various steps in the hierarchy. This treatment that employs graduated hierarchical
treatment progresses by successively reinforc- exposure along with any or all of a number of the
ing approach behavior during in vivo exposure. preceding behavioral techniques and cognitive
Once successful approach behavior is shaped techniques to address behavioral avoidance as
for a step, various steps can be chained if appro- well as catastrophic cognitions, attentional
priate, and the schedule of reinforcement can be biases, cognitive distortions, and maladaptive
thinned with the overall goal being to fade it out automatic thoughts (Beck, 1993; Beck & Clark,
completely (Davis & Ollendick, 2005; Ollendick 1997; Davis & Ollendick, 2005; Kendall, 1993).
et al., 2009a). As a result, the technique makes As a result, CBT makes use of behavioral inter-
use of reinforcement, shaping, extinction, and ventions such as reinforcement, relaxation, and
verbal feedback regarding performance (Davis modeling, but also incorporates techniques to
& Ollendick, 2005) and it has become an impor- identify and counter cognitive biases and distor-
tant standalone technique or an essential com- tions which have theoretically come to be part of
ponent of other treatment packages for specific stable, pathological psychological structures
phobia. which direct avoidance behavior and biased or
catastrophic thought (i.e., schemas; Beck (1993), being satisfied with the outcome (82.1%) and
Davis and Ollendick (2005), Farrell et al. (2019), reporting treatment occurred at a good pace
Kendall (1993), Seligman and Ollendick (2012)). (89.3%) and with no children reporting treatment
progressed too quickly (Svensson et al., 2002).
They also reported that their fear levels were
One-Session Treatment (OST) manageable during the session.
Over the past 10–15 years, there has been signifi- A successful OST session has its beginnings
cant interest in the development and use of one in the assessment of the child’s specific phobia.
variant of CBT for specific phobia: one-session An important part of the assessment process is a
treatment (OST; Davis et al., 2009b, 2012b, functional and cognitive assessment of the child’s
2019; Öst, 1987b, 1989; Zlomke & Davis, 2008). phobia during which the fear hierarchy is created,
One-session treatment is a unique combination of maintaining variables are explored, and distorted
several of the child anxiety treatments previously beliefs and catastrophic cognitions are elicited
discussed into a single, massed 3-hour session of from the child and catalogued by the clinician
in vivo exposure (Davis et al., 2009, b, 2012b, c, (for a detailed description of the functional
2019; Ollendick & Davis, 2013; Zlomke & assessment see Davis et al. (2009b, 2012c)). This
Davis, 2008). Further, OST has been deemed an functional assessment portion typically requires
empirically supported treatment and the use of 45 minutes to complete and can be supplemented
OST with children has merited well-established by additional information or confirmation from
status given the studies completed to date (see parents/caregivers at the conclusion of the assess-
Davis et al. (2019) and Farrell et al. (2019)). The ment (Davis et al., 2009b, 2012c, 2019). At the
efficacy of OST has been previously supported conclusion of the functional assessment, the cli-
by three large randomized clinical trials nician also provides the rationale for the upcom-
(Ollendick et al. 2009b, 2015; Öst et al. 2001), ing exposure session and attempts to assess the
two crossover studies (Muris et al., 1997, 1998), child’s motivation for treatment. Briefly, the
and numerous case studies (e.g., Davis et al. rationale includes a description of the exposures
(2007), and Muskett et al. (2019)). In addition, to come, termed “behavioral experiments,” reas-
large effect sizes have been found for pre- to surances that nothing will be done to the child
post-treatment differences on subjective units of without first discussing it with the child, and that
distress (SUDS; d = 1.91), BATs (d = 1.40) and the goal is not to shock, surprise, or further trau-
self-report measures of fear (d = 1.43) for chil- matize the child, but rather the clinician and child
dren receiving OST (Zlomke & Davis, 2008). will act as a team working together to overcome
the child’s fear (Davis et al., 2009b, 2012c). An
Overall Description One-session treatment is a informal assessment of the child’s motivation is
3-hour, massed cognitive-behavioral intervention also important as the clinician explains that the
during which the child is gradually exposed to child will have to experience some fear during
increasingly more fear-evoking stimuli or situa- the behavioral experiments (ideally a mild to
tions (Davis et al., 2009b, 2012b, c, 2019). The moderate amount), but that it is the clinician’s
treatment session incorporates several empiri- responsibility to ensure these are exposures that
cally supported treatment components while pro- the child will be able to handle and that if the
gressing at a pace jointly determined by the child remains in the situation instead of avoiding
clinician and child. OST makes use of graduated it that the fear will subside or at least be greatly
hierarchical in vivo exposure, PM, cognitive reduced (Davis et al., 2009b, 2012c). Ideally,
challenges, reinforcement, psychoeducation, and the functional assessment session is conducted
skills training (Davis et al., 2009b, 2012c, 2019; far enough in advance to allow for the necessary
Zlomke & Davis, 2008). This combination treat- preparations for the exposure session (e.g.,
ment has also been found to be well-tolerated by arranging for relevant stimuli or situations; Davis
children, with the large majority of children et al. (2009b, 2012c)).
Treatment Components and exposure to the stimulus (Davis et al., 2009b,

Implementation One-session treatment pro- 2012c, 2019). Finally, participant modeling can
ceeds at an irregular pace over the 3 hours of be used to break down seemingly large steps into
exposure and sessions can vary from child to smaller, more manageable steps while also
child—even when the same phobia is involved enhancing clinician support for the encounter
(Davis et al., 2009b, 2012b). There is no standard (e.g., actually touching a dog may be a roadblock
formula for structuring an OST session, other and participant modeling allows that large step to
than generally proceeding at the child’s pace— be further broken into touching the clinician
with frequent clinician encouragement—and while the clinician touches the dog and so forth).
attempting to make the session as engaging and Further, participant modeling allows the clinician
fun as possible (successful sessions with younger to remediate any skills deficits through active
children may even take the form of a turn-taking instruction in interacting with stimulus or situa-
game suggesting behavioral experiments and tion (e.g., how to approach and pet a dog without
then attempting them or other play-related activi- intimidating or scaring it; Davis et al. (2009b,
ties (Davis et al., 2009b; Kershaw et al., 2017). 2012c)). As a result, within the broader frame-
Initially, it can seem unwieldy for the clinician to work of the behavioral experiments, OST flexibly
have to incorporate cognitive challenges, PM, incorporates these various other treatment com-
psychoeducation, skills training, and reinforce- ponents fluidly (see Table 16.1 for illustration of
ment at the same time; however, exposure (i.e., a partial dog phobia treatment step-by-step
behavioral experiments) sets the stage for using description).
the various other techniques as necessary to assist
with allaying fear or educating the child (Davis
et al., 2009b, 2012c). Behavioral experiments otential Impediments to Treatment
P
generally progress in a three-step fashion: first, Success
the clinician and/or child suggest and discuss a
possible exposure; second, the clinician models A number of factors may unfortunately contribute
the proposed experiment; third, the child attempts to treatment failure or backsliding following
the modeled step, with the assistance of the thera- gains. In the four larger scale trials of CBT (i.e.,
pist, and success or failure is discussed (Davis not just OST) for specific phobia in children to
et al., 2009b, 2012c; Zlomke & Davis, 2008). date (Ollendick et al., 2009b, 2015; Öst et al.,
The other components of OST simply act as tools 2001; Silverman et al., 1999), which also targeted
in a clinician’s toolkit to address different pitfalls, other anxiety disorders than specific phobias), a
distortions, or deficits during treatment (Davis mixed picture of treatment response appears.
et al., 2009b). After agreeing on a behavioral Across all four trials, age does not seem to be
experiment, information on the distorted, and related to treatment outcome, and in the two stud-
sometimes catastrophic cognitions obtained from ies examining it, diagnostic comorbidity did not
the functional assessment are used to prompt the seem to impact the results (Ollendick et al.,
child as to what he or she predicts will happen 2009a). In two of the three OST trials, girls were
(e.g., “do you think the dog is going to bite you if found to respond better to treatment, and Öst et al.
you get closer?”) and then to discuss what really (2001) found better outcomes for animal- type
did occur following the experiment (Davis et al., phobias. Child and parent reports of depression
2009b, 2012c). Reinforcement is used through- and anxiety were found to be related to treatment
out to encourage attempts, praise success, and failure of Silverman et al. (1999); however, the
prompt further discussion; while psychoeduca- other studies do not report differences for such
tion about the feared stimulus or situation (e.g., effects or data were not specifically obtained on
how to tell a “mean” dog from a “nice” dog) these variables (Ollendick et al., 2009a). In con-
serves to remedy lulls in session progress while trast, child comorbid disorders were found to not
waiting for fear to habituate during a step while interfere with OST for specific phobias (Ryan
at the same time keeping the session focused on et al., 2017). Though unexamined in these trials,
Table 16.1 Hypothetical example of the progression of Table 16.1 (continued)

treatment for a child with a dog phobia
B. Similar procedures would occur with the second
A. First Dog (approximately 1–1.5 hours of the and third dogs (a medium and large dog respectively)
massed session) taking up the remaining 1.5 hours or until sufficient
(1) Talk about dogs; introduce idea of bringing a behavioral experiments have been conducted and
dog into the room; negotiate details of first exposure overlearned until the child exhibits little or no fear.
and assess the child’s predictions of what will Note: Treatment occurs at an uneven pace and differs con-
happen. siderably from child to child, even for the same phobic
(2) A small dog is brought into the room (e.g., a stimulus. This example was constructed with the cata-
West Highland Terrier) leashed by an assistant who strophic fear being associated with the size of the dog and
holds the leash close and tight at the opposite end of it knocking the child over and biting him or her. Reprinted
the room from the child and clinician. The clinician from Cognitive and Behavioral Practice, 16, Davis,
praises progress and encourages the child to watch Ollendick, and Öst, Intensive Treatment of Specific
the dog. They discuss how the dog’s behavior is Phobias in Children and Adolescents, 294–303, 2009,
similar or dissimilar to expectations and cognitions with permission from Elsevier.
discussed earlier.
(3) The clinician suggests moving closer. The child
declines and details are discussed. The interim is anecdotally, family variables that were initially
used to discuss educational elements regarding dogs etiological may also continue to play a role by
(e.g., Do you know how to tell a mean dog from a hampering treatment. For example, two refractory
nice dog? How can we tell if that is a mean or nice
dog?). The clinician again suggests moving closer. cases familiar to the authors involved separate
The child and clinician move 3 feet closer to the boys with specific phobias of dogs who responded
dog and discuss/challenge cognitions and quite well to treatment (i.e., both were able to
predictions. interact with dogs of various sizes on and off
(4) The clinician again suggests moving closer;
leashes by the end of treatment), but also had
however, before details can be negotiated, the child
simply begins moving forward and the therapist mothers who reported significant specific phobias
replies, “I’ll just stop when you do then; you’re of dogs as well. Both children, interestingly,
doing great!” The child and clinician move 4 more astutely noted during the functional assessment
feet closer to the dog and discuss/challenge
that a significant component to their fear was the
cognitions and predictions.
(5) The child agrees to allow the dog 2 more feet of modeling and negative information provided by
freedom on its retractable leash. their mothers. Unfortunately, the mothers were
(6) The child agrees to allow the clinician to touch not willing to undergo treatment of their own pho-
the dog. Predictions of what will happen are bias of dogs and in each case the child’s progress
assessed before and discussed following.
was noted by clinicians to suffer. OST may also
(7) The clinician uses participant modeling to have
the child come in closer proximity while the be impacted by parenting behaviors, such as over-
clinician pets the dog. protection (Capriola-Hall et al., 2020).
(8) The clinician shapes the response with praise Additionally, refractory cases may be caused by
and participant modeling until the child is the functional assessment not revealing relevant
independently petting the leashed dog.
phobic cognitions or by not incorporating relevant
(9) The child realizes how close she is to the dog’s
teeth and recoils slightly.
phobic stimuli (Ollendick & Davis, 2013).
(10) The clinician assesses the catastrophic thought In response to a lack of research addressing
(i.e., “it will bite me”), asks the child for a the effectiveness of OST in some children, a
prediction of what will happen if she pets the dog’s large-scale, noninferiority effectiveness trial of
head, and with permission demonstrates how the
OST compared to multisession CBT, the
dog dislikes having the clinician’s hand in its
mouth. The child is then encouraged to do the same Alleviating Specific Phobias Experienced by
and performance is discussed. Children Trial (or ASPECT), is currently being
(11) Etc. conducted in the United Kingdom (Wright et al.,
(continued) 2018). Projected to become the largest random-
ized control trial of specific phobias in children,
Fig. 16.1 Treatment algorithm for children with specific phobia. (Used with permission of Springer Publishing
Company, LLC, from Phobias (pp. 171–200), Cognitive Behavior Therapy for Children: Treating Complex and
Refractory Cases, 2009; permission conveyed through Copyright Clearance Center, Inc.)
Wright et al. (2018) will examine OST’s effec- Subsequently, the issue becomes what to do
tiveness and the application of treatment research when treatment is not completely effective or
to community clinicians. Numerous outcome other obstacles to treatment success arise.
measures are being used, including BATs and the Overall, a four-stage procedure is recommended
ADIS-IV C/P, as well as a 6-month follow-up for treating children’s specific phobias and
with participants and cost-effectiveness. The addressing refractory cases (Ollendick et al.,
Wright et al. (2018) randomized controlled trial 2009a; see Fig. 16.1). First, and following an ini-
should shed light on the effectiveness of OST by tial assessment, one of the preceding evidence-
community practitioners. based treatments should be selected and
implemented. If, following implementation, only References

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Separation Anxiety Disorder
in Children and Adolescents 17
Nicole E. Caporino, Joyce X. Wong,
and Arianna O’Brien Cannon
Symptom Presentation activities (e.g., sleepovers, play dates). To meet

criteria for diagnosis according to the DSM-5
The core feature of separation anxiety disorder (APA, 2013), symptoms must persist for at least
(SAD) is developmentally inappropriate and 4 weeks and cause clinically significant distress
excessive anxiety about separation from attach- or impairments in functioning.
ment figures. Youth with SAD experience dis-
tress when separating or anticipating separation
from attachment figures, worry about harm com- Prevalence and Course
ing to or losing major attachment figures, and/or
worry about experiencing an untoward event The mean lifetime prevalence estimates of SAD
(e.g., kidnapping) that results in separation from have ranged from 4% to 5% in preadolescent and
an attachment figure (American Psychiatric adult samples (e.g., Copeland et al., 2014; Kessler
Association, 2013). Youth may also resist leaving et al., 2005; Silove et al., 2015). Relative to other
home due to fear of separation, show fear of or anxiety disorders, SAD typically onsets early
reluctance about being alone at home alone, and (mean = 6–7 years old; Kessler et al., 2005; Shear
insist on sleeping near an attachment figure. Less et al., 2006) and the prevalence rate decreases
commonly, they experience nightmares involving with age (e.g., Copeland et al., 2014). Some stud-
the theme of separation (e.g., Allen et al., 2010c; ies have shown higher prevalence rates among
Cooper-Vince et al., 2014). Youth with SAD may girls than boys (Silove et al., 2015; Shear et al.,
be described as “clingy,” follow caregivers 2006) and others have found no difference (e.g.,
around at home, and cry or tantrum in an effort to Copeland et al., 2014). Among clinic-referred
avoid separation. Also, youth may frequently youth with anxiety disorders, non-White youth
“check in” with caregivers (e.g., by texting, call- have been significantly more likely than White
ing to them from another room). Because youth youth to meet criteria for comorbid SAD and
with SAD often experience intense discomfort social phobia (Kendall & Peterman, 2015). There
when apart from attachment figures, they may is some evidence that separation anxiety dispro-
refrain from engaging in age-appropriate social portionately affects youth from low-income fam-
ilies (e.g., Vine et al., 2012) and countries (e.g.,
N. E. Caporino (*) · J. X. Wong · Silove et al., 2015).
A. O’Brien Cannon
Separation anxiety in infants and toddlers is
Department of Psychology, American University,
Washington, DC, USA developmentally typical and likely adaptive; it
e-mail: caporino@american.edu peaks at 15–18 months and wanes slowly through
https://doi.org/10.1007/978-3-031-14080-8_17
250 N. E. Caporino et al.
4 years of age (e.g., Battaglia et al., 2016; Sroufe, with no anxiety disorder (e.g., Kossowsky et al.,
1997). Parental unemployment, maternal depres- 2012).
sion, and tobacco exposure in pregnancy have In line with cognitive theories of fear and anx-
been uniquely associated with high separation iety (e.g., Kendall, 1985), there is evidence of
anxiety at 1.5 years that increases through 6 years general and content-specific interpretation bias in
of age (Battaglia et al., 2016). Although the youth with SAD; when presented with ambigu-
majority of cases remit before adulthood (e.g., ous scenarios related to the threat of separation,
Foley et al., 2004), SAD warrants intervention to self-reported separation anxiety has predicted
reduce impairments in functioning that could youths’ negative interpretations (e.g., Klein et al.,
interfere with development (e.g., Foley et al., 2019). Also, there is some evidence that children
2008) and to prevent the onset of secondary dis- with fear (versus distress) disorders, including
orders (e.g., Cummings et al., 2014). Elevated SAD, exhibit an attention bias toward threat (i.e.,
separation anxiety in preschool that increases angry faces relative to neutral faces) (e.g., Waters
over time has predicted greater internalizing et al., 2014). Youth with separation anxiety com-
symptoms, worse academic achievement, and monly present with broader emotion regulation
poorer physical health throughout middle child- difficulties (e.g., with goal-directed behavior),
hood and preadolescence (Battaglia et al., 2017). which may predict increases in separation anxi-
ety over time (e.g., Schneider et al., 2018).
Although insecure attachment has also been con-
Clinical Features sidered a vulnerability for the development of
anxiety disorders, few studies have investigated
SAD is among the most common disorders diag- attachment security in relation to separation anxi-
nosed in youth who present with school refusal ety specifically (e.g., Colonnesi et al., 2011).
(e.g., Egger et al., 2003) and as many as 75% of
children with SAD exhibit some form of school
avoidance (Last et al., 1987). SAD is highly Family Factors
comorbid with other anxiety disorders (e.g.,
Shear et al., 2006). It has generally been associ- Twin studies have documented a shared environ-
ated with later anxiety disorders, including panic mental effect on SAD (e.g., Scaini et al., 2012).
disorder (e.g., Kossowsky et al., 2013) – with Along with other anxiety disorders, SAD has been
which it appears to share a genetic diathesis associated with parental overcontrol, particularly
(Roberson-Nay et al., 2012). Studies have also over-involvement and low levels of autonomy
identified SAD as a risk factor for the develop- granting (e.g., Hughes et al., 2008); decreased
ment of disruptive behavior disorders, mood dis- latency to rescue children from situations that cause
orders, and substance use problems (e.g., Silove distress (e.g., Aschenbrand & Kendall, 2012); and
et al., 2015; Brückl et al., 2007), but findings are elevated psychological control or coercive, passive-
mixed (Kossowsky et al., 2013). aggressive, and intrusive strategies for manipulating
More than 90% of youth with SAD experi- youths’ thoughts, feelings, and activities (e.g.,
ence at least one sleep-related problem (e.g., Settipani et al., 2013). Consistent with the possibil-
Alfano et al., 2007). SAD is associated with ity that parental overcontrol has a causal influence,
greater number and severity of somatic com- Kiel et al. (2016) found that extreme observer rat-
plaints (Crawley et al., 2014), and approximately ings of maternal encouragement to approach nov-
30–50% of youth with SAD complain of physi- elty (reflecting either very protective or intrusive
cal symptoms upon separating (Allen et al., behavior) were related to increases in toddlers’
2010c). Indeed, experimental research has docu- separation anxiety from 2 to 3 years old.
mented that youth with SAD exhibit exaggerated Parents of youth with SAD may also model
physiological responses to separation relative to anxious thoughts (e.g., threatening interpreta-
youth with other anxiety disorders and/or youth tions of ambiguous situations) and avoidance
17 Separation Anxiety Disorder in Children and Adolescents 251
behavior for children (e.g., Barrett et al., 1996). separation is the fear that they will not be reunited
Relative to parents of children without anxiety with attachment figures. Youth may resist separa-
disorders, they report more negative expectations tion for reasons other than fear of permanent
of their child’s skill and coping ability (e.g., separation; for example, children with social anx-
Micco & Ehrenreich, 2008). Parents’ negative iety disorder may resist separating from caregiv-
beliefs about their child’s disposition, coping ers who speak on their behalf in public, children
ability, and potential for success have been linked with OCD may resist separating from caregivers
to children’s low expectations for coping and who accommodate compulsions, and children
relatively high levels of anxiety (Herren et al., with generalized anxiety disorder (GAD) may
2013; Wheatcroft & Creswell, 2007). resist separating from caregivers who reassure
Parents often accommodate youths’ separa- them of safety. Also, worry about harm befalling
tion anxiety; for example, by sleeping in the caregivers (without a clear focus on the perma-
child’s bed, modifying their schedules to avoid nent separation that could ensue) may reflect
leaving the child with other caregivers, providing GAD or OCD and has not discriminated well
repeated reassurance when separated, and even between youth with high and low levels of sepa-
seeking part-time employment at the child’s ration anxiety (Cooper-Vince et al., 2014).
school to avoid separation (e.g., Benito et al.,
2015). Family accommodation, which is directly Behaviors exhibited by youth with SAD (e.g.,
associated with symptom severity (Iniesta- repeated reassurance-seeking) may raise concern
Sepulveda et al., 2021), is thought to maintain or about possible OCD. Youth with separation anxi-
exacerbate anxiety by interfering with the habitu- ety sometimes engage in elaborate “goodbye”
ation or violation of expectancies that would routines, which serve to delay separation, and are
occur with exposure to anxiety triggers and by distinct from compulsions. Youth with OCD are
decreasing motivation for change (e.g., Caporino, more likely to engage in rituals with intent to pre-
2020). Of the anxiety disorders, separation anxi- vent some feared outcome (e.g., harm befalling
ety has shown the strongest relationship to family parents) and typically present with multiple OCD
accommodation (e.g., Lebowitz et al., 2013). symptoms that change over time (e.g., Rettew
Both have been linked to relatively low levels of et al., 1992).
salivary oxytocin, which is implicated in the reg- A common challenge is determining when
ulation of anxiety and close interpersonal behav- multiple diagnoses are appropriate. Although
ior (Lebowitz et al., 2016, 2017). youth with SAD may defy commands to separate
Families may experience significant burden or tantrum to avoid separation, an ODD diagnosis
associated with caring for youth with SAD, par- should only be considered when there is persis-
ticularly when engaging in high levels of accom- tent oppositional behavior unrelated to anticipa-
modation (e.g., Thompson-Hollands et al., 2014). tion or occurrence of separation. In youth who
Also, mothers of children with SAD have exhib- present with GAD, important considerations for
ited lower levels of parenting self-efficacy than diagnosing comorbid SAD are whether concerns
mothers of children with social anxiety disorder, about separation occur consistently and cause
and lower levels of parenting self-efficacy and distress and impairment independent of worry
satisfaction than mothers of children without a across other domains. The DSM-5 offers addi-
disorder (Herren et al., 2013). tional guidance in differentiating SAD from other
disorders (APA, 2013).
Assessment and Diagnosis Cultural context Culture may influence symp-

tom presentation; relative to non-Hispanic White
Differential diagnosis An important consider- youth, Hispanic and Asian youth with SAD may
ation for differential diagnosis is whether the be more likely to present with somatic complaints
core fear leading to youths’ attempts to avoid (e.g., headaches, stomachaches; Gee, 2004; Pina
& Silverman, 2004). Because the extent to which absence of fear). The 34-item Separation Anxiety
youth are expected to tolerate separation varies Assessment Scale (Eisen & Schaefer, 2007) can
by culture, it is important to view a child’s behav- inform treatment planning, though published
ior in the context of demands and opportunities to reports of psychometric properties are needed.
separate from parents (APA, 2013). For example, The Separation Anxiety Daily Diary assesses the
many families do not expect children to sleep frequency of anxiety-provoking and nonanxiety-
apart from caregivers; so, bedsharing would not provoking separations, along with associated
be considered a symptom of SAD. Additionally, thoughts, feelings, behaviors, and corresponding
SAD should be distinguished from the value that parental reactions by parent (Allen et al., 2010a)
collectivistic cultures place on interdependence and child report (Allen et al., 2010b).
among family members (e.g., Triandis, 2018). Elevated scores on the 18-item Childhood
Parenting practices reflecting high levels of con- Anxiety Sensitivity Index (Silverman et al.,
trol may be normative and adaptive in some cul- 1991), which measures fears of anxiety sensa-
tural contexts (e.g., Mexican American; Varela & tions and beliefs that they have harmful conse-
Hensley-Maloney, 2009). quences, have been useful in identifying youth
with separation anxiety who are also prone to
Assessment in school-aged children and ado- panic disorder (e.g., Kearney et al., 1997). The
lescents There are many reliable and valid par- Child Anxiety Impact Scale (Langley et al., 2014)
ent- and self-report measures that could be used and the Child Anxiety Life Interference Scale
to assess separation anxiety in school-aged youth (Lyneham et al., 2013) can be used to measure
(see Table 17.1 for descriptions and psychomet- impairment across anxiety disorders, with the lat-
ric properties). The Revised Children’s Anxiety ter including an assessment of the impact on
and Depression Scale (Chorpita et al., 2005), the caregivers.
Screen for Child Anxiety Related Emotional Commonly used (semi-)structured diagnostic
Disorders-Revised (Birmaher et al., 1997, 1999), interviews, such as the Anxiety Disorders
the Spence Children’s Anxiety Scale (SCAS; Interview Schedule for DSM (Silverman &
Spence, 1998; Nauta et al., 2004), and the Albano, 1996), the Schedule for Affective
Multidimensional Anxiety Scale (March et al., Disorders and Schizophrenia for School-Aged
1997; March, 2012) have parallel parent- and Children (K-SADS; Kaufman et al., 1997), and
child-report forms and yield separate scores for the Diagnostic Interview Schedule for Children
separation anxiety among other types of anxiety. (Shaffer et al., 2000), include SAD modules.
A 30% reduction on the Separation Anxiety/ Modifications may be required to bring these
Panic scale of the parent-report MASC from pre- interviews into line with the DSM-5, though
to post-treatment can be used as a benchmark for changes to SAD criteria from DSM-IV to DSM-5
evaluating remission (Palitz et al., 2018). were minimal apart from allowing for adult onset
(APA, 1994, 2013). The Pediatric Anxiety Rating
Disorder-specific measures (summarized in Scale (RUPP, 2002) is a briefer, clinician-rated
Table 17.1) include parent- and child-report measure of anxiety symptoms across diagnoses
forms of the 12-item Separation Anxiety with cutoff scores that can be used to assess the
Avoidance Inventory (Schneider & In-Albon, progress of individual patients against the stan-
2005), which has demonstrated reliability and dard of outcomes reported in clinical trials
validity (In-Albon et al., 2013). The 20-item self- (Caporino et al., 2013).
report Children’s Separation Anxiety Scale
(Méndez et al., 2014) has been validated using a Assessment in early childhood Although SAD
large, community sample and yields scores for may onset as early as preschool age, it must be
worry about separation, distress from separation, differentiated from age-appropriate fear of sepa-
opposition to separation, and calm at separation rating from a caregiver. The use of normed
(i.e., self-confidence that is distinct from the assessments that yield separation anxiety scores,
Table 17.1 Parent- and child-report measures of separation anxiety: description and psychometric properties
Assessment Age range Informants Items and response scale Scales and psychometric properties
Anxiety measures with separation anxiety subscale
Multidimensional Anxiety Scale for 8–19 years Parent, child 9 items for Separation/ Original MASC yields scores for Separation/Panic, Physical
Children (MASC, March et al., 1997; Panic on MASC (39 items Symptoms, Harm Avoidance, and Social Anxiety as well as Total
MASC 2, March, 2012) total) and Separation Anxiety
Anxiety/Phobias on MASC 2 yields additional scores: GAD Index, Obsessions and
MASC 2 (50 items total); Compulsions, Inconsistency Index (response style), Anxiety
0–3 scale Probability Score (chance of having at least one anxiety disorder)
MASC Separation/Panic scale renamed Separation Anxiety/Phobias
on MASC 2 (“SAD scale” below)
Support for MASC four-factor model (e.g., Baldwin & Dadds, 2007)
and MASC 2 five-factor model, which excluded GAD Index due to
item overlap (March, 2012)
Norms from clinical and nonclinical samples available (Etkin et al.,
2021a, b; March, 2012)
SAD scale shows Cronbach’s alphas >.65 for child report and >.70
for parent report (e.g., Baldwin & Dadds, 2007; March, 2012; Villabø
et al., 2012)
SAD scale test-retest reliability r = .70 for parent report and .55 for
child report (Baldwin & Dadds); ICC’s (across raters) above .80 for
17 Separation Anxiety Disorder in Children and Adolescents
3-week and 3-month intervals (March et al., 1997)

Parent- and child-report MASC each predict presence and severity of
SAD in youth, with fair prediction power in youth and fair to good
prediction power in adolescents (e.g., Wei et al., 2014)
SAD scale has convergent and divergent validity for parent and child
versions (Baldwin & Dadds, 2007; March, 2012; Muris et al., 2002)
SAD scale is sensitive to treatment effects (e.g., Evans et al., 2017;
Palitz et al., 2018)
Parent-child agreement for SAD scale: r = .30–.40 (e.g., Baldwin &
Dadds, 2007; Villabø et al., 2012), corrected r = .54 (March, 2012)
(continued)
253
Table 17.1 (continued)
254
Preschool Anxiety Scale (Spence et al.), 2–6 years Parent 5 items for SAD on Yields scores for Separation Anxiety, Social Anxiety, Generalized
Preschool Anxiety Scale-Revised PAS-R (28 total); 0–4 Anxiety, OCD, and Physical Injury fears (based on results from
(Edwards et al., 2010) response scale exploratory and confirmatory factor analyses; Spence et al., 2001)
Developed with feedback from parents and experts (Spence et al.,
2001)
Some independently replicated evidence of construct validity (Etkin
et al., 2021b)
Norms from nonclinical sample available
Cronbach’s alpha generally >.70 for SAD scale (e.g., Edwards et al.,
2010)
12-month test-retest reliability: r ≥ .60 for SAD scale (Edwards et al.,
2010)
SAD subscale predicted DSM diagnosis of separation anxiety
disorder (Edwards et al., 2010)
Revised Children’s Anxiety and 8–18 years Parent, child 7 items for SAD (47 total) Yields scores for Separation Anxiety, Social Phobia, Panic Disorder,
Depression Scale (RCADS; Chorpita GAD, OCD, and Major Depression (supported by results of
et al., 2000, 2005) confirmatory factor analysis)
Cronbach’s alpha of .78 for child-report SAD scale and .87 for
parent-report SAD scale
Child-report SAD scale cutoff of 5 showed sensitivity of .73 and a
specificity of .69 for the prediction of separation anxiety disorder
Parent-report SAD scale cutoff of 4 showed sensitivity of .92 and a
specificity of .73,
Convergent and divergent validity established for child-report SAD
scale and for parent-report total score
Parent and child scores showed small, significant associations
(Chorpita et al., 2005; Ebesutani et al., 2010)
N. E. Caporino et al.
Screen for Child Anxiety Related 6–18 years Parent, child 8 items for SAD (66 Yields scores for Separation Anxiety, Panic/Somatic Symptoms,
Emotion Disorders-Revised total); 0–2 scale General Anxiety, Social Phobia, School Phobia (supported by results
(SCARED-R; Birmaher et al., 1997, of confirmatory analyses)
1999) Norms from clinical and nonclinical samples available for self-report
(Etkin et al., 2021a, b)
SAD scale has Cronbach’s alphas >.70 for child report and around
.80 for parent report (Runyon et al., 2018)
40-day test-retest reliability was moderate to high: ICC of .59 for
child-report SAD scale and .85 for parent-report SAD scale (Behrens
et al., 2019)
Cutoff score of 5 on child-report SAD scale had .76 sensitivity and
.80 specificity for identifying SAD in treatment-seeking sample
(Birmaher et al., 1997)
Cutoff score of 8 on parent-report SAD scale had .84 sensitivity and
.85 specificity in treatment-seeking sample (Van Meter et al., 2018)
Convergent and divergent validity established for child- and
parent-report SAD scale (e.g., Monga et al., 2000; Muris et al., 2002)
Child- and parent-report SAD scale is sensitive to treatment effects
(e.g., Monga et al., 2015; Muris et al., 2002)
Parent-child agreement: r = .45 for SAD subscale (Birmaher et al.,
1997)
(continued)
255
256
Spence Children’s Anxiety Scale (SCAS; 8–15 years Parent, child 6 items for SAD (38 total, Yields scores for Separation Anxiety, Panic and Agoraphobia, Social
Spence, 1998; Nauta et al., 2004) +6 filler items for child Phobia, GAD, OCD, and Physical Injury Fears (supported by results
version); 0–3 scale of confirmatory factor analysis; Orgiles et al., 2016)
Norms from clinical and nonclinical samples available for self-report
Child-report SAD subscale had Cronbach’s alpha of .70 in a
meta-analysis (Orgiles et al., 2016)
Parent report SAD subscale had Cronbach’s alpha of .74 in
nonclinical and .76 in clinical samples (Nauta et al., 2004)
Test-retest reliability: r > .75 for child report and >.80 for parent-
report SAD scale at 2-week and 3-month intervals in community
samples (e.g., Arendt et al., 2014)
Six-month test-retest reliability: r = .57 child-reported SAD in
community sample 8–12 years old (Spence, 1998)
Optimal SAD scale cutoff scores for each reporter (child = 6.5,
mother = 8.5, father = 6.5) identified youth with SAD, with
sensitivity values of at .70–.78 and corresponding specificity values
of .62–.75 (Reardon et al., 2019)
SAD subscale shows convergent and divergent validity (e.g., Essau
et al., 2002)
Parent- and child-report SAD subscale has shown sensitivity to
treatment effects (e.g., Evans et al., 2017)
Relatively high parent-child agreement on SAD subscale (e.g.,
r = .74; Brown-Jacobsen et al., 2011)
Youth Anxiety Measure for DSM-5 8–18 years Child and 6 items for SAD (50 Part I (28 items) assesses major anxiety disorders and Part 2 (22
(Muris et al., 2017a, b) parent total); 0–3 response scale items) assesses specific phobias and agoraphobia
Developed with expert feedback
Cronbach’s alpha ≥.80 for child-report SAD subscale across clinical
and nonclinical samples
Cronbach’s alpha of .84 for parent-report SAD subscale in clinical
sample
Convergent and divergent validity for total score and groups of
subscales
Parent-child agreement for SAD subscale: r = .73
(Muris et al., 2017a, b)
Disorder-specific measures
Children’s Separation Anxiety Scale 8–11 years Child 20 Yields scores for worry about separation, distress from separation,
(CSAS; Méndez et al., 2014) opposition to separation, and calm at separation (based on results of
exploratory and confirmatory factor analyses)
Validated with large samples of schoolchildren (N = 1908; N = 6016)
in Spain
Cronbach’s alpha of .88 for total scale, >.70 for every subscale
Four-week test-retest reliability: r = .83 for total score and >.65 for
every subscale
Showed convergent and divergent validity
Cutoff score of 68 showed good sensitivity and specificity for
identifying youth with SAD
(Méndez et al., 2014)
Separation Anxiety Avoidance Inventory 4–18 years Child and 12 Yields total score and 2 subscale scores, for “going to school, to bed
(SAAI; Schneider & In-Albon, 2005) parent alone” and “being or going home alone when no-one is there” (based
on results of exploratory and confirmatory factor analyses)
Cronbach’s alphas ≥.80 for child report and ≥.75 for parent report
Four-week test-retest reliability: r > .80 for parent report across
school and clinical samples; .80 for child report in school sample and
.60 for child report in clinical sample
Child-report form showed convergent and divergent validity
Children with SAD scored significantly higher on child-report form
than children with other anxiety disorders and schoolchildren

Parent- and child-report forms both showed sensitivity to treatment
change
Parent-child agreement: r ranged from .33 to .63 across samples
(In-Albon et al., 2013)
Separation Anxiety Assessment Scale N/A Child 34; 1–4 response scale Items assess fear of being alone, fear of abandonment, fear of
(Eisen & Schaefer, 2007) physical illness, worry about calamitous events, and dependence on
safety signals
May inform treatment planning
Preliminary support for the factor structure, reliability, validity, and
clinical utility of the SAAS has been described (e.g., Eisen et al.,
2011) but findings not peer-reviewed
(continued)
257
258
Separation Anxiety Daily Diary (SADD; 7–14 years Child and Daily Diary Entry Assesses the frequency of anxiety-provoking and nonanxiety-
Allen et al., 2010a) parent provoking separations, along with associated thoughts, feelings,
behaviors, and corresponding parental reactions
Content informed by a literature review and parent interviews
Compliance was acceptable for parent version
Mothers of youth with SAD reported more anxious and fewer
nonanxious separations on the daily diary than mothers of children
with other anxiety disorders and healthy children
Substantial improvement in the prediction of diagnostic group
membership was shown when SADD items assessing child symptoms
were added to information gathered from a separation anxiety
symptom questionnaire
Child version discriminated youth with SAD from healthy youth but
not youth with other anxiety disorders
(Allen et al., 2010a, b)
Note. Except for the MASC, these measures are all available to use at no cost
such as the Preschool Anxiety Scale (ages cally included some combination of
2–6 years; Spence et al., 2001), as well as struc- psychoeducation about anxiety; training in relax-
tured diagnostic interviews, such as the Preschool ation, cognitive restructuring/coping skills, and
Age Psychiatric Assessment (PAPA, ages problem-solving; exposure to anxiety-provoking
2–5 years; Egger et al., 2006), may assist with situations; and relapse prevention (e.g., Kendall
accurate diagnosis. Using machine learning & Hedtke, 2006). In efficacy trials, approxi-
tools, Carpenter et al. (2016) developed a method mately 60–80% of youth show meaningful symp-
for using the PAPA to quantify risk for SAD with tom reduction (response) and 50–70% achieve
accuracy >96% while limiting burden associated remission (the absence of the principal diagnosis
with assessment. The Child Anxiety Life following treatment) (Kendall & Peterman,
Interference Scale-Preschool Version (Gilbertson 2015). CBT protocols modified to target anxiety
et al., 2017) can be used to assess the impact of disorders in early childhood, such as the Being
symptoms on the child and caregiver(s). Finally, Brave Program (Hirshfeld-Becker et al., 2010),
the Dyadic Parent-Child Interaction Coding have shown similar response rates. Research has
System II (DPICS-II; Eyberg et al., 1994), a vali- suggested that most CBT-related symptom
dated system for coding observations during improvement happens after exposure is intro-
child- and parent-directed interactions, has been duced, with cognitive restructuring also contrib-
modified for use with young children with sepa- uting substantially to gains made by school-aged
ration anxiety and can be used at intake and to youth (e.g., Peris et al., 2015). CBT protocols
monitor progress in treatment (Pincus et al., that emphasize exposure over anxiety manage-
2006). For youth of all ages, less formal observa- ment appear to produce larger effects (Whiteside
tions (e.g., of child responses to prompts to sepa- et al., 2020).
rate for intake interviews) can corroborate other
assessment data but may not be representative of Several studies have reported findings specific
behavior outside of the clinic setting. to SAD. For example, Hudson et al. (2015) eval-
uated the family-based CBT program Cool Kids
Informant discrepancies Informant discrepan- (Lyneham et al., 2003; Rapee et al., 2006) deliv-
cies in reports of psychopathology in youth are ered in group format to youth 6–18 years old
typical and may reflect contextual variations in (N = 842) with a principal DSM-IV diagnosis of
displays of mental health concerns, reporting an anxiety disorder. The remission rate for SAD
bias, and/or measurement error (de los Reyes was 42.2% at post-treatment and 56% at 3- to
et al., 2015). There is evidence of incremental 12-month follow-up, though the protocol was
validity of cross-informants reports of separation deemed most efficacious for youth with principal
anxiety; for example, adding parent reports to GAD or OCD. The Child-Adolescent Anxiety
child self-reports (on the MASC) has increased Multimodal Study (CAMS; Walkup et al., 2008)
prediction of youths’ anxiety disorder diagnoses was a six-site, randomized controlled trial that
(Villabø et al., 2012). Parents of youth with SAD examined the relative efficacy of CBT (Coping
may be better at judging impairment whereas Cat; Kendall & Hedtke, 2006), sertraline, their
youth are more likely to report distress (Allen combination, and pill placebo for the treatment
et al., 2010c). of SAD, social phobia, and GAD in youth
7–17 years old (N = 488). CBT and sertraline
each reduced anxiety severity and their combina-
Psychological Treatment tion had a superior response rate. Although com-
bined treatment was most efficacious across all
Cognitive-behavioral therapy Given high anxiety disorders, the effect sizes relative to
rates of comorbidity, CBT studies have targeted monotherapies were the largest for youth with
SAD along with GAD and social anxiety disor- principal SAD (Cohen’s d = −0.91 to −0.98)
der. Protocols for school-aged youth have typi- compared to other principal anxiety disorders
(Cohen’s d = −0.16 to −0.69; Compton et al., individual and family-based CBT when parents
2014). Also, active treatments (CBT, sertraline, have clinical levels of anxiety (e.g., Kendall
their combination) yielded significantly greater et al., 2010). Recently, a standalone parent-based
reductions in parent-reported separation-related treatment targeting family accommodation
sleep difficulties than pill placebo, with the great- (Lebowitz & Omer, 2013) was found noninferior
est reductions reported by parents of youth whose to standard CBT based on ratings provided by
active treatment included sertraline (Caporino independent evaluators, parents, and children
et al., 2017). Acute treatment responders in (Lebowitz et al., 2020).
CAMS were less likely to exhibit chronic anxiety
across a 4-year period beginning 4–12 years after Parent-child interaction therapy Parent-child
randomization (Ginsburg et al., 2018). interaction therapy (PCIT; Eyberg, 1988) is an
Disorder-specific protocols for SAD in intervention based on both social learning theory
youth have been developed (e.g., Eisen et al., and attachment theory. PCIT incorporates child-
2008). In a waitlist-controlled trial that sam- directed interaction to strengthen the parent-child
pled youth 5–7 years old (N = 43), 76.19% of attachment as a foundation for parent-directed
children who were randomized to a 16-session interaction within a behavioral framework.
family-based CBT protocol that included Although PCIT was initially used to treat exter-
parental cognition as a treatment target no lon- nalizing problems in early childhood, it has been
ger met criteria for SAD at post-treatment adapted to treat SAD and other common anxiety
(Schneider et al., 2011). The same protocol disorders (e.g., Puliafico et al., 2013). Pilot
was compared to individual CBT in youth research and an unpublished RCT have suggested
8–13 years old (N = 64), and both programs that PCIT is efficacious in the treatment of SAD
showed medium to large effects across mea- only when it incorporates a focus on exposure
sures at post-treatment, with no significant (i.e., “bravery-directed interactions”; e.g., Pincus
group differences in remission rates at 4-week et al., 2008; Carpenter et al., 2014). The extent to
or 1-year follow-up (Schneider et al., 2013). which exposure (versus the synergy of exposure
and PCIT) explains symptom improvement is
Family involvement in CBT The majority of unclear.
youth CBT manuals incorporate caregiver ses-
sions (e.g., to promote the generalization of skills Cognitive-behavioral and attachment-based
learned in session to outside settings; Howard family therapy Attachment-based family ther-
et al., 2000). In addition to facilitating within- apy was developed to target adolescent depres-
session exposure tasks involving separation, par- sion (e.g., Diamond et al., 2002) and has been
ents may be taught contingency management integrated with CBT to target SAD, social anxi-
strategies for encouraging between-session expo- ety disorder, and GAD in adolescents (Siqueland
sure. Family-based treatment may also target et al., 2005). In addition to including all elements
parental overcontrol, rejection/criticism, anxious of standard CBT, the treatment targets parental
cognitive style and modeling, and accommoda- beliefs about anxiety, overprotection, and psy-
tion (Caporino, 2020). Although meta-analyses chological control to help the adolescent negoti-
have reported limited evidence that CBT with ate autonomy and make parent-child attachment
family involvement has added benefit over indi- bonds more flexible. Pilot research has estab-
vidual or group CBT for youth without family lished feasibility but adequately powered tests of
involvement (e.g., Peris et al., 2021), treatment- efficacy are needed (Siqueland et al., 2005).
related decreases in parental overcontrol and
family accommodation have been significantly Formats of delivery Research on nonstandard
associated with treatment outcomes (e.g., Kagan formats of treatment delivery may inform efforts
et al., 2016; Settipani et al., 2013). Also, family- to improve access to CBT for SAD. Group CBT
based CBT appears to be more efficacious than may be more cost-effective than individual CBT
and reduce the average time to intervention. computer-based CBT programs targeting anxiety
Studies that have directly compared group to in school-aged children and adolescents have
individual CBT for anxiety in youth have gener- been found superior to waitlist controls (e.g.,
ally not found significant differences in outcomes Vigerland et al., 2016; Wuthrich et al., 2012).
(e.g., Liber et al., 2008; Wergeland et al., 2014), There is preliminary support for the efficacy of
though individual CBT appears to be associated online parent-focused CBT in reducing anxiety
with larger effects than group CBT (e.g., in symptoms in youth 3–6 years old (Donovan &
waitlist-controlled trials; Reynolds et al., 2012). March, 2014; Morgan et al., 2016).
A waitlist-controlled trial of intensive 1-week Webcam-delivered CBT, which retains the
group CBT in a summer camp setting for school- real-time clinician interaction of clinic-based
aged females with SAD (N = 29) found remission treatment, has potential to increase access to
rates of 43% at post-treatment and 61% at 6-week evidence-based care when logistical constraints
follow-up (Santucci & Ehrenreich-May, 2013). (e.g., time, distance from clinic, a pandemic)
Intensive treatment in this setting may be more interfere with pursuing or continuing clinic-based
time-efficient and accessible to families for sessions. A pilot study of real-time videoconfer-
whom travel to weekly sessions would not be fea- encing CBT for SAD, social anxiety disorder,
sible, and provides opportunities for exposure to and/or GAD in youth (N = 11) established its fea-
situations (e.g., sleepovers) that could not be rep- sibility, acceptability, and preliminary efficacy
licated during a standard clinic visit. (Carpenter et al., 2018). A large-scale, federally
funded study comparing the effectiveness of
Like group CBT, computer-assisted CBT may web-based to in-person CBT for anxiety disor-
reduce the cost of treatment by reducing the time ders in youth ages 3–18 is currently underway.
burden on clinicians. Camp Cope-A-Lot (Khanna
& Kendall, 2008), a computer-assisted adapta-
tion of the Coping Cat (Kendall & Hedtke, 2006) Psychopharmacological Treatment
that requires clinician time for exposure sessions
only, has demonstrated efficacy in youth with Selective serotonin reuptake inhibitors The
SAD, social phobia, and/or GAD; in an RCT American Academy of Child and Adolescent
powered to detect moderate to large effects, there Psychiatry recommends selective serotonin reup-
were no significant differences in outcomes take inhibitors (SSRIs) or selective norepinephrine
between Camp Cope-A-Lot and individual CBT reuptake inhibitors (SNRIs) for treating anxiety
(Khanna & Kendall, 2010). Camp Cope-A-Lot disorders in children and adolescents, as these
used by CBT-naïve clinicians was also found medications are generally well tolerated and safe
superior to treatment as usual delivered in com- (Connolly & Bernstein, 2007). However, studies
munity mental health centers (Storch et al., sampling youth with separation anxiety have
2015). The internet-based BRAVE program has yielded mixed findings depending on the medica-
been found superior to a waitlist control in the tion administered. In the CAMS (Walkup et al.,
treatment of DSM-IV anxiety disorders (includ- 2008), combined CBT and sertraline yielded a
ing OCD and PTSD) in children and adolescents higher response rate (80.7%) among youth with
(March et al., 2009) and equivalent to clinic- SAD, GAD, and/or social phobia compared to
based CBT in adolescents (with power to detect CBT alone (59.7%) and sertraline alone (54.9%).
medium effects; e.g., Spence et al., 2011) – There were no significant differences between the
though the program may not be effective with monotherapies, which were each more efficacious
adolescents in routine clinical care settings (e.g., than pill placebo. An RCT that sampled 125 youth
Waite et al., 2019). There is some evidence that with these same disorders showed that 8 weeks of
the presence of SAD predicts relatively favorable a flexible dose of fluvoxamine was significantly
outcomes of BRAVE-Online, as reported by par- more efficacious than placebo (Walkup et al.,
ents and children (Spence et al., 2020). Other 2001). Birmaher et al. (2003) found fluoxetine to
be superior to placebo in the treatment of social associated with impairments in functioning as

phobia and GAD, but there were no significant well as heightened risk for developing subsequent
group differences in clinical response among anxiety disorders. SAD is most common in early
youth with SAD. childhood and may be accompanied by somatic
complaints, sleep problems, and/or school avoid-
Selective norepinephrine reuptake inhibi- ance. Parents of youth with SAD may have nega-
tors Compared to SSRIs, SNRIs have smaller tive expectations for their child’s ability to cope
effects and yield less rapid improvement in youth with anxiety and may be quick to rescue their
anxiety but are less likely to produce adverse children from distress or accommodate symp-
events (e.g., activation) than SSRIs (Mills & toms, experiencing substantial burden as a result.
Strawn, 2020; Strawn et al., 2015; Strawn et al., A multi-informant approach to the assessment of
2018). Only one RCT of SNRI medication evalu- SAD is recommended and there are well-vali-
ated efficacy for reducing anxiety in youth with dated measures of SAD symptoms in youth of all
SAD, along with other anxiety disorders (Geller ages. Research has established the efficacy of
et al., 2007). Youth with attention deficit hyperac- CBT and SSRI medication (e.g., sertraline and
tivity disorder (ADHD) and comorbid anxiety fluvoxamine) in the treatment of SAD, with their
disorders receiving atomoxetine showed combination yielding the highest response rate.
improvement in ADHD and anxiety symptoms Group CBT and computer-assisted CBT also have
after 12 weeks of treatment compared to those in empirical support and may be particularly cost-
the placebo group (Geller et al., 2007). effective, improving access to evidence- based
care for SAD. Preliminary research has suggested
Other medication classes A pilot, randomized, that webcam-delivered and intensive CBT are
placebo-controlled trial of guanfacine, an adren- also promising formats of treatment delivery.
ergic receptor agonist, in the treatment of SAD,
GAD, and social anxiety disorder demonstrated
safety and tolerability (Strawn et al., 2017) but References
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The Treatment of Generalized
Anxiety Disorder in Youth 18
Carl F. Weems and R. Enrique Varela
This chapter reviews the literature on the treat- suggestions for developmental modifications to
ment of generalized anxiety disorder (GAD) in the “how to” for younger children.
youth. We first discuss what GAD is, present key
phenomenology, and make assessment recom-
mendations. We next review the extant empirical eneralized Anxiety Disorder: Key
G
data on treatment efficacy drawing heavily upon Features
conclusions from several recent meta-analyses
and focus on cognitive behavioral therapy (CBT) The Diagnostic and Statistical Manual of Mental
techniques and procedures as they have the most Disorders-5 (American Psychiatric Association
empirical support (Silverman et al., 2008; Wang [APA], 2013) provides criteria to make an anxi-
et al., 2017; Warwick et al., 2017). In this treat- ety disorder diagnosis and differential diagnostic
ment study review, we focus on findings in terms criteria that distinguish among the anxiety disor-
of GAD treatment specifically. However, most, if ders. Generalized anxiety disorder is character-
not all, treatment studies to date have included ized by excessive anxiety and worry about a
other anxiety disorders in the samples, for exam- number of events or activities. While worry can
ple, separation anxiety disorder and social anxi- be normal (Borkovec et al., 1991; Mathews,
ety disorder, and so specific conclusions about 1990), the worries experienced in GAD interfere
GAD are limited by that fact. We make conclu- with the child’s life preventing them from, for
sions about the general efficacy of CBT for GAD example, going to or doing well in school and
and then draw conclusions about treatment effi- interfering with friendships, etc. Children may
cacy in terms of format (e.g., group versus indi- worry about their school performance, their
vidual), and discuss any differential effects for social relationships, and their health or the health
ethnicity, age, and sex as well as other predictors of others. These children may seek constant reas-
of outcome that have been reported. We conclude surance and approval from others to help allevi-
the chapter with some “hands-on” advice—how ate their worry. Most specifically impairing for
does one actually do CBT for GAD, with some youth with GAD appears to be the intensity of
their worries (Weems et al., 2000). These worries
C. F. Weems (*) may disrupt family routines (e.g., bedtime, going
Department of Human and Family Studies, Iowa to school, travel).
State University, Ames, IA, USA To be diagnosed with GAD according to
e-mail: cweems@iastate.edu
DSM-5 criteria (APA, 2013) a child must exhibit
R. E. Varela excessive anxiety. Moreover, the child or youth
Loyola University, New Orleans, LA, USA
https://doi.org/10.1007/978-3-031-14080-8_18
272 C. F. Weems and R. E. Varela
must worry for more days than not for at least duct disorder and oppositional defiant disorder
6 months about a number of events or activities from 3% to 13% and with depression from 1% to
and the child must find it difficult to control the 20% (Costello et al., 2004). Developmentally,
worry. At least one of the following physical GAD symptoms are most likely to become prom-
symptoms must accompany the anxiety or worry: inent around age 10–12 years but can be evident
restlessness, being easily fatigued, difficulty con- in children as young as 6 years (Costello et al.,
centrating, irritability, muscle tension, or sleep 2004; Weems, 2008); however, the developmen-
disturbance. The anxiety, worry, or physical tal expression of GAD symptoms may vary based
symptoms cause significant distress or impair- on other conditions such as Autism Spectrum
ment in an area or areas of functioning (e.g., Disorder (Varela et al., 2020).
social or occupational). The source of the distur-
bance is not due to physiological effects of a sub-
stance or another medical condition, and the Assessment
symptoms are not better explained by another
mental disorder (e.g., negative evaluation in We suggest using a multimethod (e.g., parent and
social anxiety disorder) (APA, 2013). child reports) multitrait (e.g., DSM-based diag-
Worry has been and continues to be a central nostic interview and worry checklist) assessment
component of the DSM definition of generalized (Weems & Stickle, 2005) to identify if treatment
anxiety disorder in children. In DSM-IIIR is warranted. In our work, we have used the
(American Psychiatric Association, 1987) unre- Anxiety Disorders Interview Schedule for
alistic or excessive worry was a major clinical DSM-IV: Child and Parent Versions [(ADIS for
feature and diagnostic criterion of Overanxious DSM-IV: C/P; Silverman & Albano, 1996) and
Disorder (OAD). The subsequent version, its previous edition (ADIS for DSM-III-R C/P;
DSM-IV (American Psychiatric Association, Silverman & Nelles, 1988)] to make diagnostic
1994) eliminated OAD and subsumed it under decisions. The Anxiety and Related Disorders
generalized anxiety disorder (GAD), but none- Interview Schedule for DSM-5, Child and Parent
theless maintained this criterion and added diffi- Versions (Albano & Silverman, in press;
culty in controlling the worry as a separate Silverman & Albano, in press), has been updated
criterion. The DSM-5 maintained these worry- for clinical practice and in research trials to pro-
related criteria (APA, 2013). Worry then is a cen- vide for differential diagnosis. This new version
tral feature of GAD with clinical significance for is based on the DSM-5 (American Psychiatric
youth with the disorder (Perrin & Last, 1997; Association, 2013), allows the ruling out alterna-
Weems et al., 2000; Songco et al., 2020). Youth tive diagnoses, and presents psychiatric disor-
with GAD also have more somatic symptoms ders. The ADIS-5 provides quantifiable data
such as restlessness, stomachaches, blushing, concerning symptoms, severity, etiology, and
palpitations, and muscle tension than youth with course of disorders. These data can be useful for
other anxiety disorders (Ginsburg et al., 2006), case conceptualization, for pre-, mid-, or post-
and research suggests youth with GAD may also treatment evaluations for tracking clinical course
have relatively more sleep problems (Alfano and response, and for research purposes. The
et al., 2007). ADIS has been the subject of several reliability
Like all the anxiety disorders, GAD is highly and validity studies (e.g., Silverman & Nelles,
comorbid with other anxiety disorders in samples 1988; Rapee et al., 1994) each demonstrating
of clinic-referred anxious youth (e.g., Weems good estimates of reliability and validity for
et al., 1998) and also in general population sam- childhood anxiety disorders. Silverman et al.
ples (see Costello et al., 2004). GAD may also be (2001) found the ADIS for DSM-IV to have kap-
comorbid with other disorders. Across studies, pas ranging from 0.80 to 0.92 for 2–3 week test-
anxiety disorder comorbidity estimates with retest reliability for separation anxiety disorder,
ADHD have ranged from 0% to 21%, with con- social phobia, specific phobia, and generalized
18 The Treatment of Generalized Anxiety Disorder in Youth 273
anxiety disorder. The ADIS has also been used in 4 = very very much). Further, children are asked
most randomized treatment studies for GAD and to rate how often (i.e., frequency) they worried
related anxiety disorders in youth (see Silverman about the item (0 = none, 1 = some, and 2 = a lot).
et al., 2008). The interview has good reliability and validity.
In addition to a diagnostic interview, we sug- For example, test-retest reliability of the WIC for
gest assessing children’s worries with a checklist the total number of worries was found to be
or worry interview. For example, Perrin and Last (r = 0.75) and for the total number of areas of
(1997) developed a 31-item worry scale based on worry was (r = 0.78), and the interview scores
DSM-III-R criteria for overanxious disorder, discriminate anxious children from non-anxious
avoidant disorder, separation anxiety disorder, children and discriminate youth with GAD from
and social phobia. Chorpita et al. (1997) have those with other anxiety disorders (see Silverman
adapted the Penn State Worry Questionnaire for et al., 1995; Weems et al., 2000).
use with children (PSWQ-C). Using a commu-
nity sample (n = 199), Chorpita et al. (1997)
examined the psychometric properties of this Cognitive Behavioral Therapy
16-item instrument and found good internal con- for GAD in Youth
sistency as well as convergent and discriminant
validity. Vasey et al. (1994) have developed a Cognitive-Behavioral Therapy (CBT) is a psy-
vignette-based interview strategy to provide a chosocial treatment that emphasizes the role of
developmental examination of the process of cognitions and behavioral learning in the devel-
children’s worries. Case vignettes were used to opment, maintenance, and amelioration of emo-
provide a context for assessing children’s ability tional problems. Cognitive behavioral therapy
to conceive of threatening possibilities, and the has several characteristics from the cognitive tra-
frequency of worrisome thoughts for each of dition (e.g., Beck, 1976) as well as from the
three hypothetical vignettes is computed. behavioral tradition (Skinner, 1953; Wolpe,
For a very brief assessment, we recommend 1958). Cognitive-Behavior Therapy is time-
the “GAD-7” which is just seven questions based limited and the typical number of sessions chil-
in part on the DSM-IV criteria for GAD and dren receive varies from around 10 to 16. While
reflects the frequency of symptoms during the CBT is conceptualized as a collaborative effort
preceding 2-week period, with these options: between the therapist and the client, it is rela-
“not at all,” “several days,” “over half the days,” tively more structured and therapist-directed than
and “nearly every day.” Data suggest the measure other therapies (e.g., client-centered therapy, play
can be validly and usefully employed with youth therapy, psychoanalysis). CBT is based on an
samples to identify GAD (see Mossman et al., educational model with the goal being to help cli-
2017). ents unlearn their unwanted reactions and to learn
We have used the Worry Interview for Children new ways of reacting. Homework is also a central
(WIC; Silverman et al., 1995) in our research feature of CBT for childhood anxiety disorders.
(Weems et al., 2000). The WIC is a semi- Cognitive therapy is based on the idea that our
structured interview and was designed to assess thoughts influence our feelings and behaviors
children’s worries in 14 areas: School, and has its roots in the work of Aaron Beck and
Performance, Classmates, Friends, War, others in the cognitive tradition (Beck, 1976;
Disasters, Money, Health, Future Events, Lang, 1977). Behavior therapy or behavior modi-
Personal Harm, Little Things, Appearance, fication is the treatment of behavioral and emo-
Family, and Other worries not covered by previ- tional disorders through the reinforcement of
ous categories. For each worry reported, the child desired behavior and suppression of undesirable
is asked to rate how much (i.e., intensity) they behavior. The behavioral techniques have their
worried about the item on a five-point scale roots in the experimental work of Ivan Pavlov
(0 = none, 1 = a little bit, 2 = some, 3 = a lot, and (respondent tradition) and B. F. Skinner (operant
tradition) as well as the applied work of Joseph attendance, intense somatic symptoms, and
Wolpe and Nathan Azrin (see Kazdin, 1978, school refusal (Pina et al., 2002; Weems et al.,
2001). Contingency management and reinforce- 2000). As noted, the literature also shows that
ment strategies, for example, follow from the children also diagnosed with GAD experience
operant conditioning paradigm while systematic more sleep-related problems (Alfano et al., 2007)
desensitization follows from the respondent para- and somatic symptoms (Ginsburg et al., 2006)
digm. These traditions (cognitive and behavioral) than clinically anxious youth without GAD.
have been largely integrated in current CBT treat- The field has advanced with demonstrated
ment manuals for childhood anxiety (Barrett, efficacy of cognitive-behavioral and pharmaco-
1998; Kendall, 1994; Silverman, Kurtines, logical strategies in the treatment of childhood
Ginsburg, Weems, Lumpkin, & Carmichael, anxiety and phobic disorders (see Albano &
1999a; Silverman, Kurtines, Ginsburg, Weems, Kendall, 2002; Creswell & Cartwright-Hatton,
Rabian, & Serafini, 1999b). Specific techniques 2007; Kendall, 1994; Ollendick & King, 1998;
are discussed further below and are outlined in Silverman et al., 2008; for a review of pharmaco-
Table 18.1. logical interventions see Walkup et al., 2002).
Anxiety disorders such as GAD in childhood Central to CBT interventions for anxiety prob-
and adolescence are highly prevalent and can lems are exposure-based anxiety reduction strate-
cause intense psychosocial impairment (Langley gies (i.e., relaxation training consisting of
et al., 2004; Silverman & Treffers, 2001). For progressive muscle relaxation and deep breathing
example, children with GAD often have diffi- paired with gradual approach to fearful stimuli
culty studying for and taking tests, poor school followed by positive reinforcement of progress
Table 18.1 Common techniques used in CBT for childhood anxiety disorders
Technique Description Example use for GAD
Graduated The basic idea is that you cannot run This means confronting the worry (i.e., fully
exposure from your problems/fears, you must processing the worry or worry-provoking
face them head on. stimulus). Worry hierarchy is developed and
therapist helps client face from least intense to
most intense.
Relaxation training Training in progressive muscle When worries arise client is instructed to do
relaxation and deep breathing. relaxation exercises.
Systematic Relaxation training paired with Condition a relaxed response to worries or worry
desensitization exposures along a hierarchy. provoking stimuli by pairing “relaxation” with
increasing levels (or hierarchy) of the worries or
worry provoking stimulus.
Self-monitoring Systematic observation and recording of Client keeps a daily record of worries and the
target behaviors. things that prompted the intense worry.
Cognitive Often termed “cognitive restructuring” Identification of the cognitive causes of the
modification- (Aaron Beck) worries in GAD and teaching of positive self-talk,
challenging An array of strategies utilized to challenging beliefs, and worry schemas. Socratic
irrational beliefs identify and restructure maladaptive and method of challenging irrational beliefs.
distorted cognitions. Empirical demonstrations of the fallacy of the
belief with the use of mini experiments and
exposure hierarchy
Contingency Designed to facilitate child graduated Contracts are written between the parent and child
management exposure by using behavioral that details the child exposure task (i.e., the step
contingency management procedures. on the hierarchy) as well as the details of the
Specific principles and procedures reward that the parent would give to the child (i.e.,
positive reinforcement, shaping, an item on the reward list) as a consequence for
extinction, and contingency contracting. successful completion of the exposure task.
Modeling The therapist acts out appropriate The client models the therapist’s positive solutions
reactions to different situations. to the worries.
through praise or tangible reinforcers). Also cen- portion of the youth participants had a primary
tral to CBT are cognitive self-control training diagnosis of GAD or OAD.
strategies (see Silverman & Kurtines, 1996). The
latter involve teaching children to self-observe, Individual Format Kendall (1994) reported the
self-talk (identify and modify), self-evaluate, and first large-scale clinical trial in which individual
self-reward (see also Kendall, 1994). child-focused cognitive-behavioral treatment
(ICBT; n = 27; ages 9 to 13 years) was found to
be efficacious relative to a waitlist control condi-
Review of Outcome Studies tion (n = 20) using a randomized design and
employing multimethod assessment and diagnos-
The number of studies examining the efficacy of tic interviews (e.g., structured interviews, multi-
psychosocial treatments for anxiety disorders in source assessment). Primary diagnoses in the
childhood has grown substantially. Overall, sample were OAD (n = 30), separation anxiety
meta-analyses and reviews of the literature sug- disorder (SAD) (n = 8), and avoidant disorder
gest that CBT is an effective treatment for GAD (AD) (n = 9). Sixty-four percent of the children in
in children and youth. Meta-analyses suggest that the treatment group no longer met criteria for an
when compared to placebo, selective serotonin anxiety disorder after treatment, whereas only
reuptake inhibitors (SSRIs) also significantly one child in the control condition no longer met
reduce primary anxiety symptoms but that ben- criteria for a diagnosis after the wait period.
zodiazepines and tricyclics are not effective in Analyses of treatment effects by diagnosis indi-
reducing anxiety symptoms. When CBT is com- cated no differential treatment effects for chil-
pared with wait-listing or no dren diagnosed with OAD versus other
treatment, CBT also improves primary anxi- diagnoses.
ety. Moreover, CBT reduces primary anxiety
symptoms more than fluoxetine, but the combi- In a similar study using a randomized design
nation of sertraline and CBT significantly reduced and employing a multimethod assessment,
clinician-reported primary anxiety symptoms Kendall et al. (1997) replicated his initial find-
and response more than either treatment alone. ings on ICBT with a larger sample (N = 94) of
However, adverse events are much more com- 9- to 13-year-old children with a primary diagno-
mon with medications than CBT and CBT is sis of anxiety: OAD (n = 55), SAD (n = 22), and
associated with fewer dropouts than medica- AD (n = 17). Participants were randomly assigned
tions (see Barrett & Farrell, 2007; Silverman to a 16-week cognitive behavioral treatment or an
et al., 2008; Wang et al., 2017). 8-week waiting-list control condition.
The majority of treatment studies that have Assessments occurred at pretreatment, mid-
included children with GAD have employed indi- treatment, post-treatment, and at 1-year follow-
vidual or group treatment formats (ICBT, GCBT) up. Results indicated that per parent ADIS

with some also including a Parent component. interview, 71.28% of the treated children no lon-
Several of these studies have included only a ger had their primary diagnosis as primary at the
small number of youth whose primary diagnosis end of treatment and 53.19% no longer met crite-
was GAD or OAD (e.g., Nauta et al., 2003; Wood ria for their primary anxiety disorder at post-
et al., 2006; Bogels & Siqueland, 2006; Öst et al., treatment based on either parent or child ADIS
2001; King et al., 1998; Heyne et al., 2002). interviews. Gains were maintained at 1-year fol-
Although no study has focused solely on the low-up for most dependent variables. By com-
treatment of GAD, several have included a rela- parison, only two of the children in the waitlist
tively large number of youth diagnosed with condition no longer met criteria for their primary
GAD. In the following sections we review this anxiety disorders at the end of the waitlist period.
literature with a focus on studies in which a large Kendall et al. (1997) also examined treatment
effects by diagnosis. They concluded that there
were no overall differences in treatment effects end of the treatment period. Treatment effects by
among OAD, SAD, and AD. However, there diagnosis were not reported.
were significant Diagnoses by Trials interactions Two other studies have examined the efficacy
in predicting the mother report STAIC-P and the of ICBT in comparison to group cognitive-
CBCL internalizing scale with simple main behavioral treatment (GCBT) (Flannery-
effects tests revealing reductions only for the Schroeder & Kendall, 2000; Manassis et al.,
OAD and SAD groups. Another interaction in 2002). Flannery-Schroeder and Kendall ran-
predicting TRF internalizing scale scores was domly assigned 8- to 14-year-old anxious chil-
also significant with reductions in scores only for dren to one of three conditions: 18-week ICBT
the OAD group. (n = 13), 18-week GBCT (n = 12), or 9-week
Barrett et al. (1996) examined the efficacy of waitlist (WL) (n = 12; treated after the waitlist
the CBT approach developed by Kendall and col- period). Primary diagnoses were GAD (n = 21),
leagues with an Australian sample of clinically SAD (n = 11), and SoP (n = 5). Results showed
anxious 7- to 14-year-old children: OAD (n = 30), that 73% of the children in the ICBT group and
SAD (n = 30), and Social Phobia (SoP) (n = 19). 50% of the children in the GCBT group did not
The children were randomly assigned to one of meet criteria post-treatment for their primary
three 12-week conditions: CBT (n = 28), CBT anxiety disorder. Only 8% of the children in the
plus a parent component referred to as FAM WL condition did not meet criteria for their pri-
(CBT + FAM) (n = 25), or a waiting-list (WL) mary anxiety disorder at post-treatment.
condition (n = 26; treated after the waitlist Differences between the two treatment condi-
period). 69.8% of the children (n = 37) in the tions and the WL condition were significant, but
treatment conditions no longer met criteria for an the two treatment conditions were not significant
anxiety disorder following treatment compared from each other. In addition, 64% of children in
to 26% of the children (n = 6) in the WL condi- the ICBT group and 50% of children in the GBCT
tion after the waiting period. There was also a dif- group no longer met criteria for any anxiety dis-
ference between the treatment conditions with order following treatment. At 3-month follow-up,
84% of the children in the CBT+FAM condition 79% of children in ICBT and 53% of children in
no longer meeting criteria compared to 57% of GBCT did not meet criteria for their primary
the children in CBT alone condition. This differ- diagnosis and 50% of children in ICBT and 53%
ence was no longer significant at a 6-month fol- in the GBCT did not meet criteria for any anxiety
low-up but was significant again at a 1-year disorder (GAD, SAD, and SoP). Treatment
follow-up with 70.3% of the children in the CBT effects by diagnosis were not reported.
group no longer meeting criteria for an anxiety Manassis et al. (2002) randomly assigned 78
disorder compared to 95.6% of the children in the clinically anxious 8- to 12 year-old children to a
CBT+FAM group. Barrett et al. did not find sig- 12-session ICBT (n = 41) condition or a
nificant differences in the treatment outcome by 12-session GCBT (n = 37) condition. In both
type of pretreatment diagnosis (GAD, OAD, and conditions, parents received a parent training
SoP). program. Primary diagnoses were GAD (60.3%),
Dadds et al. (1992) had also demonstrated that SAD (25.6%), simple phobia (SP) (6.4%), SoP
CBT+FAM (n = 7) was superior to a waitlist con- (6.4%), and Panic Disorder (1.3%). Both condi-
dition (n = 7) in a relatively small sample of 7- to tions were shown to lead to significant improve-
14-year-old anxious youth: OAD (n = 10), SAD ments in parent and child report measures, and
(n = 4), with five of the seven children in the only clinician ratings varied by treatment group
treatment condition no longer meeting criteria for with clinicians rating the ICBT group as showing
an anxiety disorder diagnosis at post-treatment. more gains than the GCBT. Independent of treat-
All seven children in the waitlist condition con- ment condition, children with GAD showed more
tinued to meet criteria for an anxiety disorder at gains by mothers than children with other
diagnoses.
In sum, ICBT has been shown efficacious to there was no differential effect for type of pri-
waitlist controls in a number of well-designed mary anxiety diagnosis, comorbid child depres-
randomized control studies with samples consist- sion and parent depressive symptoms were
ing of a large portion of youth diagnosed with associated with less favorable outcomes (see
GAD/OAD. In addition, where ICBT was com- Berman et al., 2000). We review additional pre-
pared with GCBT, there were no consistent dif- dictors of efficacy in the next section.
ferences, but when differences were found, these
favored ICBT. Similarly, when outcomes were
compared by diagnosis, there appears to be fairly Predictors of Treatment Outcome
inconsistent results. However, when differentials
in gains were found, these tended to be relatively Of the ICBT and GCBT studies targeting GAD
better results for youth whose primary diagnosis reviewed above, most examined potential moder-
was GAD/OAD. ating effects of some key demographic and
related variables on treatment outcomes. No
Group Format A group format has also shown moderating effects were found for gender
efficacy for the treatment of GAD. Barrett (1998) (Silverman, Kurtines, Ginsburg, Weems,
was the first to demonstrate that group cognitive- Lumpkin, & Carmichael, 1999a; Silverman,
behavioral treatment (GCBT; n = 23) was effica- Kurtines, Ginsburg, Weems, Rabian, & Serafini,
cious relative to a waitlist control condition 1999b; Manassis et al., 2002), or age and comor-
(n = 20) (ages 7 to 14 years). Primary diagnoses bid status (Silverman, Kurtines, Ginsburg,
were: OAD (n = 30), SAD (n = 26), and SoP Weems, Lumpkin, & Carmichael, 1999a;
(n = 4). The percentage of children who were Silverman, Kurtines, Ginsburg, Weems, Rabian,
improved (i.e., no longer met DSM-III-R criteria & Serafini, 1999b; Kendall et al., 1997). Only
for any anxiety disorder) was significantly greater one study found main effects for treatment out-
for children in GCBT (74.8%) than for children comes based on gender and age (Barrett et al.,
in the waitlist control condition (25.2%). 1996). Specifically, for females, the CBT+FAM
Treatment effects by diagnosis were not reported. condition was more effective than the CBT alone
condition at the end of the treatment and at 1-year
Silverman, Kurtines, Ginsburg, Weems, follow-up. Younger children (7–10 years) had
Lumpkin, and Carmichael (1999a) also used a higher rates of diagnosis-free participants at post-
randomized clinical trial to evaluate the efficacy treatment and at 1-year follow-up in the
of group cognitive behavior therapy (GCBT) ver- CBT+FAM condition compared to young chil-
sus a waitlist control condition to treat GAD dren in the CBT alone condition. The older chil-
(n = 8; or 22% of the completers in the sample dren (11–14 years) did not show differences in
had GAD); OAD (n = 17; 46% of the sample); or treatment effects across outcomes.
SoP (n = 12; 32% of the sample). Results indi- Of the studies reviewed, only Silverman,
cated that GCBT was efficacious in producing Kurtines, Ginsburg, Weems, Lumpkin, and
and maintaining treatment gains (youth in GCBT Carmichael (1999a) included a sufficient number
showed substantial improvement on all the main of ethnic minorities, mostly Hispanic/Latino
outcome measures. These gains were maintained (n = 26), to examine moderating effects of ethnic-
at 3-, 6-, and 12-month follow-up and youth in ity on treatment outcomes. They found that eth-
the waitlist control condition did not show nicity did not moderate treatment effects. A
improvements from the pre- to post-wait). In par- second study by Silverman, Kurtines, Ginsburg,
ticular, using the ADIS-C/P diagnoses, 64% Weems, Rabian, and Serafini (1999b) also
(16/25) of the participants in GCBT were recov- included a sufficient number of Hispanic/Latino
ered at post-treatment (i.e., no longer met pri- youth for conducting moderation analyses.
mary diagnoses); 12.5% (2/16) in the waitlist However, this second study was focused on chil-
condition were recovered at post-wait. Although dren with phobic disorders of whom 14% had a
comorbid diagnosis of GAD. Two subsequent pleted). Primary diagnoses of completers were
studies combined the two samples from the GAD (n = 5), SoP (n = 2), and SP (n = 2). The
Silverman studies (Silverman, Kurtines, GBCT protocol was 10 weeks and based on the
Ginsburg, Weems, Lumpkin, & Carmichael, work of Silverman, Kurtines, Ginsburg, Weems,
1999a; Silverman, Kurtines, Ginsburg, Weems, Lumpkin, and Carmichael (1999a); Silverman,
Rabian, & Serafini, 1999b) and reanalyzed those Kurtines, Ginsburg, Weems, Rabian, and Serafini
data to examine the equivalence of treatment (1999b). At post-treatment, three of the four
effects across Hispanic/Latino and white non- youth in the GCBT condition no longer met crite-
Latino youth (Pina et al., 2003) and potential ria for their primary diagnosis and one of the five
moderating effects of ethnicity and other child youth in the AS condition no longer met criteria
individual characteristics and parent mental for their primary diagnosis.
health in treatment outcomes (Berman et al., Berman et al. (2000) examined a number of
2000). Although the samples for these two stud- potential moderators of treatment outcomes of
ies include children with a large portion of other exposure-based CBT with data from Silverman,
anxiety disorders in addition to GAD, we review Kurtines, Ginsburg, Weems, Lumpkin, and
them considering the scarcity of research in this Carmichael (1999a); Silverman, Kurtines,
area with ethnic minorities. Ginsburg, Weems, Rabian, and Serafini (1999b).
Pina et al. (2003) examined the efficacy of They found that comorbid diagnoses of depres-
exposure-based cognitive treatments on 6- to sion (assessed through the ADIS, C/P), depres-
16-year-old Hispanic/Latino youth (n = 52) and sive symptoms (measured with the Children’s
European American youth (n = 79). Primary Depression Inventory, CDI; Kovacs, 1981), and
diagnoses for the Hispanic/Latino youth were trait anxiety (measured with the State Trait
GAD/OAD (n = 10), SAD (n = 4), SoP (n = 10), Anxiety Inventory for Children – Trait Version,
SP (n = 23), and other (n = 5). Primary diagnoses STAIC; Spielberger, 1973) at pretreatment were
for the European American youth were GAD/ associated with treatment failure, defined as not
OAD (n = 15), SAD (n = 4), SoP (n = 7), SP having “‘recovered’ (i.e., no longer meeting cri-
(n = 46), and other (n = 7). Results indicated that teria for the DSM diagnostic criteria for the pri-
84% of Hispanic/Latino youth and 83.9% of the mary and targeted phobic or anxiety disorder).”
European American youth no longer met criteria Parents’ global severity ratings on the Symptom
for their primary diagnosis at post-treatment and Checklist-90 (SCL-90; Derogatis, 1983), par-
these percentages were statistically equivalent. ents’ symptom scores on the obsessive-
Treatment effects were also equivalent between compulsive, psychoticism, depression, hostility,
the two cultural groups in clinically significant and paranoia subscales of the SCL-90, parents’
improvement and child- and parent-completed self-rating of depression (measured with the
questionnaires. Treatment gains over time (3-, 6-, Beck Depression Inventory, BDI; Beck et al.,
and 12-month follow-ups) were also generally 1961), and parent self-ratings of anxiety (assessed
equivalent across the two groups in most mea- with the Fear Questionnaire; Marks & Matthews,
sures, with one exception. The European 1979) at pretreatment were also associated with
American youth reported more gains over time treatment failure as defined above. Age, income,
through the use of the Revised Children’s and primary anxiety diagnosis were not predic-
Manifest Anxiety Scale (RCMAS; Reynolds & tors of success or failure in therapy.
Richmond, 1978). In addition, children’s scores on the STAIC
One other study has focused on ethnicity in and parents’ global severity score on the SCL-90
the treatment of GAD using GCBT. Ginsburg and and scores on the depression, hostility, obsessive-
Drake (2002) randomly assigned 12 African compulsive, and paranoia subscale of the SCL-90
American 14- to 17-year-old adolescents to a at pretreatment were associated with poor out-
GBCT condition (n = 6; 4 completed) or an atten- comes gauged by a lack of a drop of 4 points or
tion and support (AS) condition (n = 6; 5 com- more on an 8-point clinicians’ severity scale.
Children’s scores on the CDI and STAIC and par- family composition, and a measure of therapeutic
ents’ scores on each of the subscales of the SCL- relationship did not have an effect on treatment
90 predicted post-treatment clinicians’ ratings of outcome.
symptom severity (i.e., more than 5% of variance In all, the available literature indicates little or
in severity ratings explained) for those involved no differential effects of ICBT and GCBT for
in individual treatment, whereas only the chil- GAD based on demographic variables (i.e., gen-
dren’s scores on the RCMAS and externalizing der, family income, and ethnicity) and primary
subscale of the CBCL were predictive of severity anxiety diagnosis, but other variables appear to
ratings for those in group treatment (i.e., more affect treatment outcomes. Specifically, comor-
than 5% of variance explained). SCL-90 global bid depression, severity of anxiety symptoms,
severity rating and scores on the depression, hos- and parental psychopathology each have tended
tility, somatization, paranoia, obsessive-to be associated with poorer outcomes. In addi-
compulsive, and psychoticism subscales of the tion, although effective across ages, CBT-based
SCL-90 predicted clinician’s ratings (i.e., more treatments may be even more effective for
than 5% of variance explained) of symptom younger children with GAD. Better attention to
severity at post-treatment for children under moderators and mediators of efficacy is needed in
12 years old. For adolescents (12 years or older), the next generation of outcome studies.
CDI scores and parents’ scores on the internaliz-
ing scale of the CBCL and parents’ score on the
RCMAS were predictive of severity ratings (i.e., Practical Suggestions
more than 5% of variance explained). for Implementing CBT for Youth
Southam-Gerow et al. (2001) also examined with GAD
potential effects of a number of child, parent, and
environmental characteristics on treatment out- For clinicians new to the treatment of anxiety in
comes, specifically good treatment response (i.e., youth, we would suggest using one of the excel-
not meeting criteria for any anxiety disorder lent guides for professionals (e.g., Silverman &
based on ADIS -P) versus poor treatment response Kurtines, 1996) and parents (reviewed in Weems,
(i.e., meets criteria for one anxiety disorder 2005). For example, the text Treating Anxious
immediately after treatment (n = 135) or at 1-year Children and Adolescents by Rapee, Wignall,
follow-up (n = 107) based on ADIS -P). They et al. (2000) was designed for professionals and
combined the samples from the Kendall (1994) presents their insights that they have gained from
and Kendall et al. (1997) studies and reanalyzed years of research and clinical work at their anxi-
those data (85% of total N for their analyses) in ety disorders research center and clinic. The goal
combination with new data collected in the same of the text is to provide mental health profession-
anxiety clinic (15% of total N for their analyses). als with understandable and detailed suggestions
Pretreatment primary diagnoses were OAD or for conducting effective treatment procedures.
GAD (59%), SAD (24%), and SoP or AD (17%). Although not a treatment manual, the book pro-
They found that higher scores on the withdrawn vides sample treatment programs designed for
subscale of the Child Behavior Checklist and different clinical contexts (i.e., the authors’ typi-
higher scores on the Anxious/Depressed subscale cal program, a managed care setting, and an
of the Teacher Report Form were associated with extended treatment setting) with illustrative case
poor treatment response immediately following studies. Rapee, Spence, et al. (2000) is a compan-
treatment and at 1-year follow-up. In addition, ion book for parents. An excellent chapter on
being older was associated with poor treatment conducting exposure with youth with GAD can
response immediately following treatment and be found in Davis et al. (2020).
mother depression (measured by the BDI) was Table 18.1 delineates some of the common
associated with poor response treatment at 1-year techniques used in CBT for GAD. In the follow-
follow-up. Ethnicity, gender, family income, ing we provide some specific suggestions for
doing treatment for youth with GAD. While CBT on empathetic understanding of the goals and
is directive we always take time to develop rap- desires of the client (both child and family).
port with the child and their family and part of The therapist also tries to foster a sense of uni-
this work is done during the assessment process. versality about worry and youths develop a worry
Participants in our intervention work with anxi- hierarchy in the initial session. Use of a worry
ety disorders including GAD first learn about interview can facilitate the ranking of the various
anxiety in general. To do this the therapist pres- worries from least to most fear provoking/inter-
ents a cognitive and behavioral conceptualization fering/intense. Later in treatment the therapist
of anxiety (see Silverman & Kurtines, 1996 for will utilize various techniques (e.g., relaxation
more detailed instructions). It is explained to cli- training) and client education (contingency man-
ent and his or her mother and father that when we agement) to help the client face increasingly
are afraid or anxious, fear or anxiety is evident in intense worries along the hierarchy.
three main ways: (l) body reactions, such as heart We next begin to teach relaxation techniques.
beating fast, etc., (2) cognitions (e.g., talking to After the child has mastered the relaxation tech-
oneself, such as “I might fail”), and (3) behav- niques (with in-session and homework assign-
iors, in particular, we avoid the feared object or ments), the relaxation techniques are then
event. We also explain that worry is natural practiced during imagined exposure to the initial
because it helps us to plan for the future and or lower level hierarchy items. The goal of these
anticipate future danger; however, when it gets sessions is to create a context where youth can
too intense it can interfere with our ability to do practice their relaxation skills while “facing” or
well in school or prevent us from doing the things approaching items on the stimulus hierarchy. We
we would like to do. find that homework assignments are facilitated
The therapist also takes time to explain the by parental involvement, and depending on the
importance of exposure or approach behavior. age of the child we often include parents in the
With GAD it can be more difficult to help the cli- therapy sessions (i.e., with younger children par-
ent conceptualize this in terms of worry. “How ents tend to spend more time in the session). In
am I supposed to approach my worry?” youth addition, we also hold a parents-only time at the
and parents may wonder. We explain that we will end where the procedures are taught to parents.
approach the things that make us worry (school, In addition to pairing exposures with relax-
tests) and confront the worries. For a child who ation, we use contingency management proce-
worries about crime or world events, this means dures. This includes positive reinforcement,
talking about the specific concerns and process- shaping, extinction, contingency contracting, fol-
ing the worry fully. Often worries are maintained lowing through, and consistency. In particular,
by a superficial contemplation of the true dangers performance of in-session and out-of-session
involved. exposures along the fear hierarchy is facilitated
In initial sessions youth are given an overview by the use of contingency management.
of the treatment and the therapist tries to create Specifically, contracts are written between the
the sense that therapy is a joint effort between the parent and child that detail the child exposure
counselor and the youth to help them worry less task (i.e., the step on the hierarchy) as well as the
and to help them so that the worry no longer details of the reward that the parent would give to
interferes with their life. The overall rationale the child (i.e., an item on the reward list) as a con-
might be explained as being able to worry appro- sequence for successful completion of the expo-
priately and so the emphasis is on mastery but not sure task.
perfection (i.e., no worry at all is an unreasonable Sessions then begin to focus on hierarchy
goal). The joint effort is facilitated by using the exposure tasks (i.e., gradual exposure to items on
first session to develop a therapeutic alliance (i.e., the hierarchy combined with relaxation and con-
emphasis in the initial sessions should also focus tingency contracting), with self-efficacy building
(i.e., therapist praise at success along the
h ierarchy and self-praise at successes), and con- ious youth and their definitions with GAD-related
tinued relaxation training practice. We introduce examples are presented in Table 18.2 (See also
the concept of self-evaluation as deciding whether Weems et al., 2007).
or not one is satisfied with his/her accomplish-
ments. Sports examples are used to help youth Table 18.2 Common negative thoughts experienced by
learn the concept of shaping (or gradual learn- anxious youth
ing). For example, it might be explained that it GAD-related
would not be reasonable to expect to hit a three- Negative cognition Definition examples
point shot in basketball every time you shoot or Catastrophizing Expecting the Worries that
even in every game. worst possible if it rains
outcome of an there will be
Youth are helped to make a list of possible event or situation a flood.
rewards that the youth might receive (e.g., get to News story
go to the park with mom; extra playtime after about crime
school; points toward a tangible reward). An means
robbers are
emphasis on verbal self-rewards is part of our going to
work with older youth and children who are par- break into
ticularly motivated. Examples might include: the house at
“I’m really proud of myself,” “I really handled night.
Overgeneralizing Believing that a One difficult
that well,” “I can handle it if I try,” “Good going,”
single negative test results
and/or “Great Job!” The importance of believing outcome is in worries
in one’s self is emphasized as well. The therapist representative of or that school
explains how we should reward or praise our- will occur in all will always
similar future be awful.
selves for even partial successes (shaping). That
events.
is, we will praise ourselves for partial successes Personalizing Attributing control A team loss
as well, not just for the “three-point shot.” The over the outcome results in
focus is on the idea that no one does everything of negative events persistent
perfectly and not doing something 100% per- to internal causes. worries that
“the team
fectly should not mean that you should not praise lost the
yourself. game
We next begin cognitive modification work. because of
Some therapies do this cognitive training before me.”
Selective Focusing on only Worries that
exposures are begun (Kendall, 1994). This may
abstraction the negative she/he
be more appropriate for older youth who can aspects of an ruined the
understand the abstract issues involved. We have event. whole
found that the exposures often provide concrete recital/game
because of
examples so that children understand the cogni-
one little
tive component better. Thus, doing the cognitive mistake.
work as exposures progress is one developmental Anxiety The beliefs that A racing
modification to CBT that therapists may wish to sensitivity anxiety-related heart rate
try. Cognitive modification is also often termed sensations (such as leads to
heart beat worries that
“cognitive restructuring” (Beck, 1976) and is awareness, they have
really a vast array of strategies utilized to identify increased heart heart
and help restructure maladaptive and distorted rate, trembling, problems.
cognitions. Such strategies include the identifica- shortness of
breath) have severe
tion of negative thoughts, images, and beliefs and negative social,
the teaching of positive self-talk, self-observation, psychological, or
challenging beliefs and schemas, and self- physical
evaluation. Common negative thoughts in anx- consequences.
Cognitive modification strategies might the child’s worries. The extant empirical data on
include challenging the above irrational or erro- treatment efficacy suggests that cognitive behav-
neous beliefs by demonstrating the logical fal- ioral therapy (CBT) techniques and procedures
lacy of the belief or by empirical demonstrations have excellent empirical support (Silverman
of the fallacy of the belief. For example, we use et al., 2008). While the treatment studies to date
mini experiments and the exposure-hierarchy to have included other anxiety disorders in the sam-
demonstrate that the result a child expects from ples evaluated, we concluded that GAD can be
the worry (e.g., social ridicule) does not always effectively treated with CBT. Moreover, treat-
happen. However, the period from childhood to ment efficacy does not appear to vary by format
adolescence is characterized by changes in the (e.g., group versus individual), ethnicity, and
way a child is able to process information (e.g., gender. However, there is some evidence to sug-
young children are often not conscious—or as gest that comorbid depression and parental men-
conscious—of their threat evaluative thoughts tal health may decrease efficacy. We concluded
and are often unable to articulate their cognitive the chapter by providing some hands-on sugges-
experience in a way that lends itself to easy iden- tions in the implementation of CBT for GAD in
tification of their anxiety-related cognitions). youth based on our intervention experience.
Trying to identify anxious cognitions such as
catastrophizing or attempting to have the child Author Note Dr Weems is supported by grants from the
monitor catastrophizing thoughts in such cases US Environmental Protection Agency, (Award 84004001),
National Institute of Justice (2019-R2-CX-0013), the
will often prove unhelpful to the therapeutic Office on Violence Against Women (2017-SI-AX-0004),
process. and the Youth Policy Institute of Iowa, as well as contracts
In our work with younger children (see e.g., with the state of Iowa (Child Support Training BOC-
Weems & Carrión, 2003), we start from a “teach- 18-003; Service Training FOSU-21-001; and Community
Partnership for the Protection of Children ACFS21088;
ing adaptive cognitions” framework. That is, the prime sponsor for each is HHS-US Department of Health
focus is simply on teaching verbal (cognitive) & Human Services). The content is that of the authors and
statements that are adaptive. In the case of chil- the content does not necessarily reflect the opinions, find-
dren with GAD the idea is teaching statements ings, and conclusions of any funding source or agency.
The authors declare no conflict of interest.
that counteract avoidance and promote facing
your worries. For example, the therapist might
ask the child with GAD, “What can you say when
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Selective Mutism
19
Karin L. Price, Natalie Delgado,
and Kelly N. Banneyer
Introduction tion, etiology, and treatment practice with other

anxiety disorders (Muris & Ollendick, 2015).
Selective mutism (SM) is an anxiety disorder in As per DSM-5 criteria for SM, the child’s
which children are unable to speak in certain inability to speak in public settings must be ongo-
social contexts where it is expected of them (e.g., ing for at least a month and not be better explained
school), while they are able to speak in other by any other symptoms of psychosis, neurodevel-
more comfortable settings, such as at home. An opmental, or speech disorders (2013). These chil-
initial conceptualization of SM is thought to orig- dren do not fail to speak due to an intellectual
inate from the German physician Adolf Kussmaul deficit, as they are easily capable of speaking to
who described the condition in the nineteenth people with whom they feel comfortable, such as
century as aphasia voluntaria, or “a voluntary their immediate family members. The prevalence
absence of speech” (Kussmaul, 1877 in Driessen of SM has been found to be 0.03–0.79% in the
et al., 2020). In the 1930s, a Swiss child psychol- population, with a higher rate among girls than
ogist coined the term elektiver Mutismus (Tramer, boys (Bergman et al., 2002). This relatively rare
1945 in Driessen et al., 2020), and the condition condition typically has an age of onset between 2
became known as “elective mutism.” Elective and 5 years of age (Kristensen, 2000; Sharkey &
mutism was first included in the third edition of McNicholas, 2012) and is highly comorbid with
the Diagnostic and Statistical Manual of Mental other disorders, especially social anxiety (69%)
Disorders (1980) within the category of “Other (Driessen et al., 2020). Additionally, one study on
Disorders of Infancy, Childhood, or Adolescence” the comorbidity of SM and language disorders
and the term was updated to “selective mutism” found that 81% of children with SM had speech
in the DSM-IV (1994) to indicate that the condi- and language disorders (Klein et al., 2013).
tion is not elected freely by an individual but
instead present in certain, selective contexts. The
DSM-5 (American Psychiatric Association, Conceptualization
2013) reclassified SM in the category of “anxiety
disorders” given overlap in symptom presenta- While somewhat controversial, the reclassifica-
tion of SM as an anxiety disorder was borne out of
a substantial number of studies describing the
K. L. Price (*) · N. Delgado · K. N. Banneyer
overlap between SM and other anxiety disorders
Department of Pediatrics, Baylor College of
Medicine, Houston, TX, USA in terms of symptomatology and etiology, as well
e-mail: klprice@bcm.edu as very high levels of comorbidity between SM
https://doi.org/10.1007/978-3-031-14080-8_19
288 K. L. Price et al.
and other anxiety disorders (Driessen et al., 2020). there is a lack of published quantitative data on
Given this relatively recent re-classification, and nonbehavioral approaches. Given data regarding
that SM most often has its onset in the early child- effectiveness of Cognitive Behavioral Therapy
hood years, it is helpful to consider a functional (CBT) for other childhood anxiety disorders,
analysis of the behavior associated with this diag- CBT is the treatment approach most frequently
nosis. That is, mutism in situations where speech used to treat SM. Reviews of the SM treatment
is expected is an avoidance behavior. As such, literature over the past 25 years (e.g., Viana et al.,
SM can be conceptualized as a pattern of avoid- 2009; Zakszeski & DuPaul, 2017) reveal that
ance of anxiety-provoking situations that has been more than 95% of published studies incorporate a
strengthened over time through negative rein- behavioral approach, and most use multiple
forcement. When the child with SM is mute, oth- behavioral strategies within each treatment.
ers in the environment typically remove the However, SM presents unique challenges that
demand for speech, thus negatively reinforcing require typical anxiety-focused CBT approaches
mutism as a response in situations where speech to be modified. SM has an earlier age of onset
is expected and anxiety-provoking. than most childhood anxiety disorders, requiring
This cyclical pattern is similar to that seen in developmental modifications to anxiety treat-
other childhood anxiety disorders, and under- ments. In addition, children with SM often fail to
standing it is extremely helpful when designing speak to the therapist at the onset of treatment.
and implementing a treatment plan for children Both of these differences necessitate unique strat-
with SM. This cycle usually begins when a child egies for child engagement and caregiver involve-
with SM is asked a question or prompted to speak ment throughout the treatment process. Finally,
in some way. This results in anxiety-provoking children with SM tend to experience the most
thoughts (such as “What if I sound strange?” functional impairment in the school environment
“What if I don’t know the answer?” or “What if (Bergman et al., 2008), thus requiring treatment
they won’t stop asking me questions?”) and/or involvement of and coordination with school
feelings including emotional responses (such as personnel.
anxiety, fear, or nervousness) or physiological In recent years, several randomized control
responses (such as increased heart rate, nausea, trials (RCTs) have demonstrated that behavioral
headache, or sweatiness). To reduce these uncom- therapy is effective at reducing symptoms of SM
fortable thoughts and feelings, the child will then (Cornacchio et al., 2019; Bergman et al., 2013;
avoid the situation by remaining silent. Many Oerbeck et al., 2013), with effects maintained for
times, an adult may “rescue” the child by speak- many children up to 5 years post-treatment
ing for them or removing the expectation to (Oerbeck et al., 2018). Behavioral approaches to
speak. When the expectation is removed, the treating SM target the underlying function of
child experiences a sense of relief, which results speech being withheld (i.e., to escape anxiety
in negative reinforcement of the mute behavior. and/or speech demands). A variety of behavioral
Because of this, the child will then have an treatments have been studied in individual fami-
increased chance of avoiding speech the next lies (Bergman et al., 2013), caregiver-child dyads
time a prompt for speech in an uncomfortable (Catchpole et al., 2019), intensive therapy groups
situation occurs. (Cornacchio et al., 2019), and caregiver-focused
formats (Oerbeck et al., 2013). Successful inter-
ventions have been administered in clinic set-
Intervention tings, focused on schools, facilitated with mobile
apps (Bunnell et al., 2018), or incorporated a
Psychosocial Treatment multimodal approach (Klein et al., 2016). While
several specific treatments have been investigated
Outcome comparisons among various psychoso- with strong evidence of effectiveness, there are
cial treatment approaches for SM are difficult, as general behavioral principles that are utilized
19 Selective Mutism 289
nearly universally. These will be summarized rective. For example, in their two-session
here. intervention using mobile apps, Bunnell et al.
(2018) used a structured shaping hierarchy and
Psychoeducation contingency management protocol that included
Psychoeducation involves teaching children and immediate rewards for successive approxima-
their caregivers about factors maintaining symp- tions of speech beginning in the first visit. In
toms of SM and providing an overview and ratio- Social Communication Anxiety Treatment
nale for behavioral intervention. Emphasis is (S-CAT; Mulligan & Shipon-Blum, 2015), the
placed on helping families understand the rela- therapist is intentionally “nonchalant” during ini-
tion between anxiety and avoidance, the role of tial interactions, reducing pressure on the child to
avoidance in maintaining anxiety, and the process speak and increasing comfort by not expecting
of exposure treatment. Examples from the indi- the child to look at the therapist. Similarly,
vidual child/family situation are used to facilitate Oerbeck et al. (2018) use “defocused communi-
understanding and engagement. During the psy- cation,” during which the therapist sits beside
choeducation phase of treatment, caregivers are rather than opposite the child, creates joint atten-
also coached through identifying ways that their tion using an activity the child enjoys, “thinks
own behavior reinforces their child’s avoidant aloud” rather than asking the child direct ques-
responding/mutism via accommodation. tions, gives the child enough time to respond
rather than talking for the child, continues the
Initial Treatment Interactions dialog even when the child does not respond ver-
Early stages of behavioral treatment for SM can bally, and tries to receive a verbal answer in a
be quite difficult, especially in cases where a neutral way rather than praising the child. In
child has rarely spoken outside the home. Initial Parent-Child Interaction Therapy for Selective
treatment interactions that target increasing Mutism (PCIT-SM; Carpenter et al., 2014), inter-
speech between the child and the therapist are vention first focuses on teaching caregivers Child
important in setting the stage for successful Directed Interaction (CDI) skills to help the child
behavioral intervention. That is, there is a careful warm up in a new situation before verbal demands
balance between eliciting and reinforcing speak- are made. Exposure skills are introduced after
ing behavior, while deliberately avoiding nega- comfort has been achieved, using Verbal Directed
tive reinforcement of mutism. Differential Interaction (VDI) skills.
attention to speaking behaviors is often used,
with nonverbal avoidance behaviors (e.g., point- raduated Exposure: Shaping,
G
ing or nodding) being ignored. Given the young Prompting, and Modeling
age of many children presenting for SM treat- Exposure-based interventions form the backbone
ment, initial sessions are often play-based and for treatment of most childhood anxiety disorders
include activities, games, and toys that are both (Higa-McMillan et al., 2015). In the context of
pleasant and designed to elicit speech. At this SM, exposure treatment includes practicing
stage, any attempt at vocalization or verbaliza- speaking behavior in settings (e.g., school, in
tion (e.g., whispering directly into a caregiver’s community locations), with people (e.g.,
ear while the therapist is in the room) is attended extended family members, teachers, peers), and
to and rewarded. At times, intervention must start in situations (e.g., when ordering food or needing
with merely reinforcing speaking behavior in the help) where comfortable speech does not cur-
treatment setting, even without the therapist rently occur. Notably, exposure practices are
present. explicit and agreed upon by the child, without
Different behaviorally-based SM treatment any intent to “catch” the child with SM speaking
approaches handle initial interactions between unawares. The goal of exposure-based treatment
the child and the therapist in unique ways, rang- is for the child to engage in brave speaking
ing from highly directive to intentionally nondi- behavior because she has decided to face her
fears, not because she has been tricked into mouths (e.g., blowing), mouthing sounds or
speaking in a new situation or with a new words, or vocalizing phonemes, whereas others
person. can begin treatment by responding with words.
Most often, initial exposure practices involve The therapist frequently prompts speech during
speaking in front of and then to the therapist, with the shaping process, usually encouraging the
later exposures taking place at school and in other child to use words to communicate, speak with
community settings. During the initial phases of louder volume or in a more typical voice, and
treatment, the therapist takes primary responsi- extend the duration of speech.
bility for directing most aspects of the treatment, Hierarchies typically expand along several
including exposure exercises. However, one of dimensions, with the choice of dimension
the guiding principles of behavioral treatment for depending on the child’s presentation and treat-
SM is that this responsibility or “control” should ment goals (see Figs. 19.1 and 19.2). Sample
be gradually transferred to caregivers or teachers dimensions include: from speaking directly to a
and, to the extent possible, to the child (Bergman caregiver to speaking directly to the therapist,
et al., 2013). Thus, later exposures or “homework from responding to categorical questions to
assignments” are often facilitated by caregivers answering open-ended questions, from respond-
and school personnel in between visits with the ing to questions to asking questions, from whis-
therapist. pering to full volume, and from planned to
Exposure-based hierarchies must be individu- spontaneous speech. Once consistent and sponta-
alized, based on the child’s current patterns of neous speech with the therapist has been estab-
speaking behavior. Shaping is often used in SM lished, a child can then become an active partner
treatment, with the therapist reinforcing succes- in generating ideas for expanding exposures.
sive approximations of the desired outcome – Similar to other exposure-based therapies, fear
comfortable speech. Some children’s initial thermometers and fear ladders are useful tools
“brave talking hierarchies” or “talking ladders” for generating exposure ideas. Strategies for early
begin with making non-word sounds with their in-session exposures include naming games (col-
Fig. 19.1 Sample hierarchy for initial fading in therapist

Fig. 19.2 Sample hierarchy for initial use of voice and increasing volume
ors, animals), counting, and structured games Once the child is engaging in regular, audible
with “rules” for verbal components (e.g., during speech with the therapist, exposures then move
Candyland, the player must name the color of the outside of the therapy room to begin to gain eco-
card chosen or during Uno the player must name logical validity. Such exposures must occur with
the color and number on each card played). the permission of the parent, and no identifying/
Children often then progress to answering cate- protected health information is shared during
gorical questions using a set formula, such as: practices (e.g., child’s name or diagnosis). Most
of the time, it is advisable for the parent to be
1. The therapist asks an open-ended question present during exposures so they can learn the
(What is your favorite color?) and waits 5 sec- steps for conducting exposure practices and what
onds for a response. to so when a practice does not go as anticipated,
2. If the child does not respond, the therapist as well as model confidence in their child’s abil-
repeats the question in a forced choice format (Is ity to be brave and provide praise for successful
your favorite color pink, purple, or something practices. In a shared treatment setting (such as a
else?), again waiting 5 seconds for a response. clinic or shared office), children with SM are
3. If no response happens, the therapist takes a often engaged in exposures with confederates in
step back in the hierarchy (e.g., caregiver asks the setting, including colleagues, students, and
the question and child responds to caregiver) office personnel. Children are prompted to
until a successful exposure is completed. answer or ask general questions (e.g., “what is
4. All verbalized responses receive gentle praise your favorite color?” or “what is your favorite
and rewards (see Contingency Management animal?”). Where possible, in-session exposures
below). may also expand to gift shops, food courts, coffee
stands, information desks, and other situations important treatment component. That is, it is
that prepare caregivers for facilitating exposures often imperative to identify a treatment liaison or
outside of session. The therapist begins to actively partner in the school setting who can facilitate
coach caregivers in facilitating exposures, includ- exposures. School-related exposure situations
ing establishing a plan for practice with the child, may include the parking lot, carpool line, school
executing the exposure, problem-solving poten- entryway, classrooms, hallways, offices, play-
tial barriers, and rewarding success. grounds, “specials” areas (music, art, library),
For some children with SM, initial out-of- and the cafeteria. Expectations for speaking in
session exposures may include practices with school generally involve peers, teachers, admin-
extended family members with whom they do not istrators, and other personnel. Stimulus fading, or
currently speak comfortably. These exposures “sliding in,” is an important tool in school-based
can be completed via telephone, video chat, voice exposures.
or video recordings, or in person and often follow
the same sequence of exposures completed in timulus Fading/Sliding In
S
session. Community-based exposures may Stimulus fading involves systematically increas-
include asking/answering questions at grocery ing the difficulty of an exposure by gradually
stores or general merchandise stores (e.g., Target, adding in new stimuli. In SM treatment, this usu-
Walmart). For example, a child may be chal- ally begins with fading or “sliding in” a new per-
lenged to ask “How much does this cost?” in son into a situation where the child is already
order to earn a treat, or encouraged to ask a store talking to a trusted person. This mechanism can
clerk a question (e.g., “Where is the cereal be used to facilitate the child using speech with
aisle?”). Children with SM can complete expo- the therapist early in treatment by fading the ther-
sures that include ordering their own drinks, apist into a room where a child with SM is talk-
meals, or treats at restaurants, ice cream shops, ing/playing with a caregiver. Stimulus fading is
donut shops, etc. Such exposures are best facili- used in conjunction with ongoing rewards and
tated when planned and practiced with the thera- prompts for speech as agreed upon by the child,
pist or caregivers in advance, before entering the caregiver, and therapist during collaborative hier-
in vivo situation. Once in the situation, the child archy building.
with SM may require coaching or additional Stimulus fading is an important mechanism in
practice with the caregiver in order to be success- school-based exposures, where the goal is for
ful. As a general rule, caregivers should be teachers, peers, and other school personnel to
encouraged to try to end every exposure practice become part of the population of people with
with an accomplishment, even if the accomplish- whom the child speaks regularly. Children with
ment is not the end goal of the practice that was SM are often mute in the general school setting,
planned. For example, if the planned exposure is even with caregivers, siblings, and others with
for a child to order her own ice cream and she whom they speak comfortably outside of school.
freezes, the caregiver can instead change to a cat- A child with SM may need to start the sliding in
egorical question by asking, “Would you like process at school by getting comfortable speak-
chocolate or vanilla ice cream?” and praise an ing with their caregiver in the school setting,
audible verbal response. which may include the parking lot, school
Exposures in the school setting follow a simi- grounds, or entryway before advancing to the
lar graduated pattern as established in session classroom. Once in the classroom, a teacher or
and in the community. However, as caregivers other identified school-based liaison may “fade
typically cannot remain in the school environ- in” or “slide in” to the setting. This may include
ment for long periods of time, and given that chil- having the caregiver and child play verbal games
dren are likely to respond differently when their or read books aloud in an empty classroom while
caregiver is present in the school setting, exten- the liaison enters the room and sits far away from
sive engagement with school personnel is an the interaction. The liaison may then gradually
move closer to the interaction, eventually joining arate from exposure-based intervention or a use-
in. Once the child is comfortable with this sce- ful step in a fear hierarchy, the use of audio and
nario and speech is audible and comfortable, a video recordings can be quite helpful in SM
new stimulus is introduced. For example, a peer treatment.
selected by the child may be asked to join in a
verbal game, question and answer session, or Contingency Management
reading circle that the child has been practicing Contingency management is often used to sup-
with her teacher. Over time, other classmates port exposure-based practices for children with
may be invited to join the small group until the SM. It includes positive reinforcement of desired
child can speak and read aloud to her entire class. behaviors (i.e., rewards for speaking) and lack of
Stimulus fading in a school setting must often reinforcement for undesired behaviors (i.e.,
be accompanied by educating teachers and school ignoring silence or nonverbal responding).
personnel about SM, including the general Interventions for SM most often include rewards
importance of encouraging independent speech for steps toward treatment goals, including those
from the child and ignoring or discouraging non- completed in-session, during planned between-
verbal avoidance behaviors. In addition, peers session exposures, and spontaneous instances of
and teachers may benefit from coaching on using brave talking. In many behavioral models of
“light praise” rather than overly enthusiastic or intervention, rewards are introduced at the outset
potentially embarrassing positive attention for of treatment and typically include immediate
new speaking behaviors. reinforcers that are inherently valuable in the
moment (e.g., stickers for preschool-aged chil-
Self-modeling dren) or understood to be part of a token econ-
In prior SM treatment paradigms, self-modeling omy (e.g., “Brave Bucks,” reward tickets or
has been discussed as a useful component, some- points). Families are encouraged to develop a
times distinguished from exposure-based prac- rewards list and, over time, to establish an
tice in that the procedure is specifically designed “exchange rate” that makes sense given the fre-
to maximize the child’s identification as a com- quency of reinforcement.
fortable speaker and increase self-efficacy (Kehle Negative reinforcement plays a large role in
et al., 1998). For SM treatment, self-modeling maintenance of SM symptoms, in that the relief
involves making an audio or video recording of a that occurs when the demand for speech is
child as he speaks in a comfortable situation. The removed in the face of a child’s silence (e.g., the
recording is then played in a low-frequency speaker moves on or someone else answers for
speaking situation with the child present. In some the child), is highly rewarding. During SM treat-
interventions, video splicing is used to create a ment, caregivers and others in the child’s envi-
video in which the child comfortably answers ronment (e.g., siblings, teachers, and peers)
questions that appear to be posed by a new adult should be coached in removing accommodations
(e.g., classroom teacher) within the same video for nonverbal responding. Accommodations typi-
“conversation.” There are various free, user- cally include responding for the child, accepting
friendly video editing software programs (e.g., nonverbal responses (e.g., nodding, pointing),
Avidemux [Windows and Mac compatible], and “giving up” during planned exposure prac-
iMovie [for Mac users], VSDC Free Video Editor tices. Relatedly, classroom-based accommoda-
[for Windows users], Splice for mobile platforms, tions that allow for nonverbal responding (e.g.,
etc.) that can be used to create these videos. Some communication boards, use of notes or gestures/
evidence suggests that video self-modeling, signals) should be reserved for situations related
when combined with stimulus fading and rein- to health and safety (e.g., restroom need, illness/
forcement, produces meaningful changes in injury) and faded out over time.
speech in a short time period (Bork & Bennett, Finally, a response cost component can be
2019). Regardless of its conceptualization as sep- added to exposures, particularly when it occurs
somewhat naturally in an exposure situation. For rigorous methodology and case reports suggest
example, a child may be coached to complete an benefits, good tolerance, and high parental
exposure that includes ordering her own drink at acceptability.
a restaurant. If she is able to order her drink, she Manassis et al. (2016) completed a systematic
may have whatever drink she chooses. If she is review of the evidence for the use of pharmaco-
not able to do so, the caregiver will order water therapy in reducing symptoms of SM in children,
instead. In this instance, a natural reinforcer or including only studies with >2 participants.
disincentive is provided for speaking or not Symptomatic improvement was found for 66/79
speaking, respectively. children treated with SSRIs, with fluoxetine
being the most frequently prescribed medication.
In addition, 4/4 children treated with an MAO
Psychopharmacology inhibitor demonstrated improvement. Reporting
on tolerability was inconsistent across studies,
There is limited information regarding treat- and the duration of follow-up assessments was
ment options for children who demonstrate per- highly variable.
sistent symptoms of SM despite engaging in In an attempt to overcome some of the limita-
evidence- based psychosocial intervention. tions in the extant literature on pharmacotherapy
Therefore, clinicians often look to the broader of SM, Barterian et al. (2018) completed a ran-
literature on treatment of childhood anxiety dis- domized, single-case, multiple-baseline design to
orders, including psychopharmacology. For examine the effects of fluoxetine on symptoms of
example, the Childhood Anxiety Multimodal social anxiety and speaking behavior in 5 chil-
Study (CAMS; Compton et al., 2014) indicated dren with psychosocial treatment-resistant SM.
that children with moderate to severe anxiety All children demonstrated reduced social anxiety
disorders benefitted most from a combination of symptom severity and improvements in speaking
CBT and serotonin- specific medication (i.e., behavior during this 12-week trial, and overall
sertraline). parental acceptability ratings were high. Of note,
Applying this evidence to SM should be done all five children continued to meet diagnostic cri-
with caution, as SM has several features that dis- teria for SM after the 12-week trial.
tinguish it from other anxiety disorders of child- Limitations in the literature suggest that clini-
hood. For example, the onset of SM is typically cians treating children with SM should approach
younger than in other anxiety disorders, and the possibility of pharmacotherapy carefully,
many providers lack experience in treating young using a risk-benefit analysis for each case. While
children with medication. In addition, traditional most studies show that the potential benefits of
psychosocial interventions that are very effective medication typically outweigh the risks in child-
with other childhood anxiety disorders (e.g., hood anxiety disorders (Bridge et al., 2007),
Coping Cat; Kendall & Hedtke, 2006a, b) require studies of the risk and benefit specifically for
significant modification to apply to children with children with SM are significantly lacking. In
SM. We may expect medication interventions to addition, optimal dosage, timing of medication,
require similar modification. and guidance on timelines for discontinuation are
There is a dearth of evidence regarding effi- currently nonexistent. Overall, the body of evi-
cacy of medication in treating children with SM, dence suggests that exposure-based CBT alone
and studies that exist have significant limitations should be considered a “first line” treatment for
including small sample size, lack of comparison most children, particularly those of preschool
groups, and minimal blinding. Most studies are age. Medication may be reserved for those with
single case reports or twin studies, and heteroge- who do not respond to a trail of a strongly
neity of study design and outcome measures evidence- based psychosocial treatment and
make it difficult to amass evidence across studies should likely be used in combination with ongo-
(Manassis et al., 2016). Smaller studies with less ing CBT.
Other Considerations (Elizur & Perednik, 2003; Bradley & Sloman,

for Assessment and Intervention 1975; Steinhausen & Juzi, 1996). These findings
are consistent with the clinical experience of
Temperament those working with a larger number of children
with SM, particularly in diverse practice
Temperament is an important component to locations.
include in conceptualizing SM. First, behavioral Some authors have noted concern with possi-
inhibition is a vulnerability factor for the devel- ble over-diagnosis of SM in bilingual children
opment of childhood anxiety, including SM secondary to the “silent period” or nonverbal
(Muris et al., 2016). Children who demonstrate period that is seen as a frequent and normal part of
behavioral inhibition have persistent shyness and second language acquisition in youth. The dura-
fearfulness of new situations and around new tion of this silent period is typically less than
people. Behavioral inhibition is closely tied to 6 months, but it can last for up to a year, during
social anxiety, which is a prominent feature of which time the child may refrain from speaking in
children with SM (Muris & Ollendick, 2015). the new language until they feel comfortable
In addition to behavioral inhibition, parents communicating in it. When this learning period
sometimes report strong-willed and oppositional persists, parents, teachers, and clinicians may
behaviors in their children with SM, including stub- begin to suspect SM, even when silence in the set-
bornness, irritability, argumentativeness, noncom- ting of the new language may be developmentally
pliance, and tantrums (Ford et al., 1998). Researchers appropriate. Thus, assessors may need to consider
have found that as many as 29% of youth with SM whether the silent period persists out of the typi-
have oppositional defiant disorder (Yeganeh et al., cal time frame for language acquisition, in the
2006), while others may exhibit more mild behavior presence of anxiety or shyness, and most impor-
difficulties (Cohan et al., 2008). At this time, it is not tantly if the difficulties in speaking is not only evi-
clear whether oppositionality is a symptom of SM dent in the new language but also in their home
or a comorbidity (Bubier & Drabick 2009; Drabick language (Toppelberg et al., 2005). At the same
et al., 2010). Regardless, understanding the possible time, early intervention is important for reducing
temperamental differences among children with interference and impairment from SM symptoms,
SM contributes to more effective intervention, with and it is not advised to systematically delay treat-
treatment components to address social anxiety and ment for second language learners presenting
oppositional behaviors available to supplement with possible SM. Understanding bilingual lan-
intervention directed specifically at reducing symp- guage development is necessary to correctly diag-
toms of SM. nose SM in second language learners.
Additionally, it is proposed that acculturation
status of the parents may be a risk factor for the
Linguistic and Cultural development of SM (Elizur & Perednik, 2003).
Considerations Parents’ and caregivers’ level of assimilation,
language acquisition, and cultural acceptance
Given the relatively low prevalence of SM, lin- may be additional risk factors to consider that
guistic and cultural factors have not received sig- may impact whether a child develops SM, and
nificant attention. As indicated previously, how and when to best intervene.
children with speech and language disorders are
at higher risk for the development of SM (Starke,
2018), consistent with the diathesis-stress model Conclusion
of anxiety development. Similarly, data indicate
that immigrant/bilingual children have a higher Selective mutism is a relatively rare childhood-
prevalence of SM diagnosis as compared to onset anxiety disorder that is characterized by a
monolingual children across international groups failure to speak in some social situations despite
typical verbal communication in other settings. tive mutism: A randomized controlled pilot study.
Behaviour Research and Therapy, 51(10), 680–689.
Left untreated, SM can have a significant impact Bork, P., & Bennett, S. (2019). Video self-modeling, fad-
on children’s social functioning and academic ing, and reinforcement: An effective treatment pack-
achievement. Treatment for SM typically age for children with selective mutism. Clinical Child
includes a modified version of exposure-based Psychology and Psychiatry, 25(2), 446–455.
Bradley, S., & Sloman, L. (1975). Elective mutism in
Cognitive Behavioral Therapy (CBT), which has immigrant families. Journal of the American Academy
been consistently demonstrated to be an effective of Child Psychiatry, 2, 510–514.
treatment for other childhood anxiety disorders. Bridge, J. A., Iyengar, S., Salary, C. B., Barbe, R. P.,
Specific CBT-based interventions for SM most Birmaher, B., Pincus, H. A., Ren, L., & Brent, D. A.
(2007). Clinical response and risk for reported suicidal
often used include psychoeducation and expo- ideation and suicide attempts in pediatric antidepres-
sure (including behavioral principles of shaping, sant treatment. JAMA, 297(15), 1683–1696.
prompting, modeling, stimulus fading, and con- Bubier, J. L., & Drabick, D. A. G. (2009). Co-occurring
tingency management). Parent/caregiver involve- anxiety and disruptive behavior disorders: The roles
of anxious symptoms, reactive aggression, and shared
ment in treatment is paramount, and treatment is risk processes. Clinical Psychology Review, 29,
typically most effective when school-based per- 658–669.
sonnel can be engaged as treatment collaborators. Bunnell, B. E., Mesa, F., & Beidel, D. C. (2018). A two-
Temperament, language, and cultural factors are session hierarchy for shaping successive approxima-
tions of speech in selective mutism: Pilot study of
important considerations in diagnosing and treat- mobile apps and mechanisms of behavior change.
ing SM. Finally, supplemental treatment with Behavior Therapy, 49(6), 966–980.
medication may be considered for older children Carpenter, A. L., Puliafico, A. C., Kurtz, S. M., Pincus,
and those who demonstrate a limited response to D. B., & Comer, J. S. (2014). Extending parent–child
interaction therapy for early childhood internalizing
psychosocial interventions. problems: New advances for an overlooked popula-
tion. Clinical Child and Family Psychology Review,
17(4), 340–356.
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Treatment of Social Anxiety
Tracy L. Morris and Johann D’Souza
Transitory shyness is particularly common venue, it is not surprising that the school context
among very young children, and a large segment is a significant source of distress for children and
of the population will experience symptoms of adolescents with SAD (Blöte et al., 2015). As
social anxiety at some point across the lifespan. children often do not have the freedom to avoid
However, for some, the experience of social anxi- school and other feared social situations, parents
ety is pervasive and leads to substantive distress and teachers may misinterpret clinging and cry-
and impairment. Social anxiety disorder (SAD; ing as oppositional behavior rather than as a
also known as social phobia) is defined as a symptom of social anxiety, and as such appropri-
“marked fear or anxiety about one or more social ate intervention is delayed or denied. For those
situations in which the individual is exposed to for whom more covert cognitive or physiologic
possible scrutiny by others” (SAD; American modes predominate, parents may be unaware of
Psychological Association, 2013, p. 118). The their child’s distress until the condition becomes
classic symptom constellation includes height- quite severe and comorbid conditions such as
ened physiologic reactivity (e.g., increased heart depression and substance abuse lead to pro-
rate and muscle tension), cognitions reflecting nounced changes in functioning. For instance,
negative evaluation (e.g., “Everyone is looking at one study found that if social anxiety is left
how stupid I am.”), and overt escape and avoid- untreated, it gets worse over adolescence, per-
ance and avoidance behaviors (e.g., school haps because parents have less of a role in encour-
refusal, reticence to speak), although primary aging their children to participate in activities,
response modes vary considerably across indi- while at the same time school and social demands
viduals. As school is children’s primary social are increasing (Hoff et al., 2017).
T. L. Morris (*)
West Virginia University, Morgantown, WV, USA Epidemiology
e-mail: tracy.morris@mail.wvu.edu
J. D’Souza Lifetime prevalence estimates for SAD range
Menninger Department of Psychiatry and Behavioral
Sciences, Baylor College of Medicine, Houston, TX, from 5.0% to 12.1% in the United States depend-
USA ing on the sampling procedures and methods of
Department of Psychology, University of Houston, assessment employed, with a greater prevalence
Houston, TX, USA in females (Ruscio et al., 2008; Grant et al.,
Texas Institute for Measurement, Evaluation, and 2005). Studies in other Western countries show
Statistics, Houston, TX, USA similar prevalence rates (Iancu et al., 2006). A
https://doi.org/10.1007/978-3-031-14080-8_20
300 T. L. Morris and J. D’Souza
national survey found that 9% of adolescents met anxiety include the interaction of multiple factors
criteria for lifetime SAD with a higher p revalence (Spence & Rapee, 2016; Wong & Rapee, 2016).
in females (Burstein et al., 2011). Social anxiety Primary proposed risk factors include genetic
disorder often begins in childhood or early ado- predisposition, physiologic reactivity, parenting
lescence (Chavira & Stein, 2005). It is possible style, and peer socialization. Behavioral inhibi-
that the increased social demands and capacity tion (a tendency to approach new situations with
for self-awareness that occur during adolescence restraint, avoidance, and distress) is thought to
may result in symptoms of shyness crossing the have an inherited biological component, and
threshold into SAD during this developmental higher rates of SAD have been found among chil-
stage. It also may be the case that age of onset dren previously classified as behaviorally inhib-
estimates has not been entirely accurate due to ited (see Hirshfeld-Becker et al., 2008 for
the relatively limited research on the expression review). Experiential avoidance is another mech-
of social anxiety in young children, which in turn anism that has been identified as contributing to
may be due to the paucity of developmentally social anxiety (Epkins, 2016).
appropriate assessment measures (see Morris A growing literature base has implicated the
et al., 2004). role of parenting in the development and mainte-
Over the lifetime, SAD is frequently comor- nance of SAD. For example, one study found that
bid with a range of other psychiatric conditions unsolicited physical assistance by mothers was
from mood disorders to substance use disorders. associated with greater child social anxiety
However, SAD is especially comorbid with (Morris & Oosterhoff, 2016). Results from
anxiety- related disorders such as agoraphobia another study suggest that parents’ negative
(32.4%), generalized anxiety disorder (32.0%), beliefs about anxiety are related to increased
panic disorder (27.2%), and separation anxiety parental accommodation, which is then related to
disorder (27.4%; Burstein et al., 2011). Children increased child anxiety severity (Johnco et al.,
and adolescents who experience extreme levels 2021). Children and adults with social anxiety
of social anxiety have lower levels of peer group have described their parents as engaging in over-
acceptance and fewer close friendships (Greco & controlling behavior and restricting social inter-
Morris, 2005; La Greca & Lopez, 1998; Morris, action (Anhalt & Morris, 2008; Greco & Morris,
2001), which may help set the stage for a down- 2002). Laboratory investigations have found par-
ward spiral leading to depression. Adolescents ents of socially anxious children to demonstrate
may turn to alcohol and other substances in an more controlling and rejecting behavior toward
attempt to self-medicate and feel less inhibited in their children during joint interaction tasks than
social situations—and their subsequently more parents of non-anxious children (Greco & Morris,
socially gregarious behavior is reinforced by 2002; Hummel & Gross, 2001; Rork & Morris,
peers which in turn leads to increased substance 2009). Parents of anxious children have been
use (Blumenthal et al., 2010; Essau et al., 1999). found to model threat interpretations to ambigu-
Social anxiety disorder is likely to be a chronic ous cues and to provide and reinforce avoidant
condition in the absence of direct intervention solutions in response to hypothetical social sce-
(Yonkers et al., 2001). narios (Bar-Haim et al., 2007; Brumariu & Kerns,
2008; de Rosnay et al., 2006; Hane et al., 2008;
Lewis-Morrarty et al., 2012). Outside the home,
Causal Factors the quality of children’s peer relationships has
been found to be associated with social anxiety,
As with most psychiatric disorders, no single though it is often difficult to ascertain whether
causal path has been identified for SAD. Rather, lowered peer acceptance is a cause or conse-
explanatory models for the development of social quence of anxiety-related behavior (Erath et al.,
20 Treatment of Social Anxiety in Children and Adolescents 301
2007; Greco & Morris, 2005; La Greca & Lopez, nxiety Disorders Interview Schedule
A
1998; Morris, 2001; Storch et al., 2005). Some for DSM-IV Child/Parent Version
research has suggested that children and adoles- (ADIS-C/P; Silverman & Albano, 1996)
cents who are socially anxious underestimate
their own level of social skill and focus—to their The ADIS-C/P provides thorough coverage of
detriment—on perceived errors in social behavior anxiety disorder symptom clusters and also
(Higa & Daleiden, 2008; Inderbitzen-Nolan screens for the presence of affective and disrup-
et al., 2007). In addition, the perception of social tive behavior disorders. The social phobia section
acceptance may be as or more important than of the ADIS-C/P asks the child (and parents—
actual social acceptance. One study in a clinic- who are interviewed separately from the child) to
referred sample of youth found that youth self- provide fear, avoidance, and interference ratings
perception and mother-perception of social across 13 social and performance situations.
acceptance were independently associated with Intensity ratings are included to assess the extent
social anxiety even after controlling for depres- to which social fears interfere with daily
sion (Epkins & Seegan, 2015). Another interest- functioning.
ing study found that social support and social
self-efficacy are uniquely associated with lower Self-report Measures
SAD symptoms, and social support even has a Self-report questionnaires are integral to the
statistically significant effect on reducing SAD assessment of children over 8 years of age. The
symptoms after a negative life event (Aune et al., most extensively validated and widely used self-
2021). report measures of social anxiety are the Social
Anxiety Scale for Children-Revised, the Social
Anxiety Scale for Adolescents, and the Social
ssessment of Social Anxiety
A Phobia and Anxiety Inventory for Children.
in Children and Adolescents
Proper assessment is necessary not only for pur- ocial Anxiety Scale for Children-
S
poses of diagnostic classification, but in order to Revised (SASC-R; La Greca & Stone,
generate useful targets of change for inclusion in 1993)
treatment plans—and to adequately evaluate
treatment outcome. When evaluating children The SASC-R is a 22-item measure comprised of
and adolescents, it is important to obtain infor- three factors: fear of negative evaluation, social
mation from multiple sources. Due to the covert avoidance and distress with new or unfamiliar
nature of many aspects of social anxiety, parents peers, and more generalized social avoidance and
should not be considered the gold standard for distress.
information about their children in this matter
(De Los Reyes et al., 2010). Since context mat-
ters, teachers and peers may be the most appro- ocial Anxiety Scale for Adolescents
S
priate sources of information regarding a child’s (SAS-A; La Greca & Lopez, 1998)
performance in school and interactions with
peers. A multi-contextual assessment strategy The SAS-A parallels that of the SASC-R. Scores
will help guide case conceptualization and treat- on the SASC-R and SAS-A have been found to
ment planning, and the most commonly employed correlate with peer sociometric data and mea-
methods for the assessment of social anxiety in sures of self-esteem. Research conducted by
children and adolescents are presented briefly Reijntjes et al. (2007) found SASC-R scores
below. were predictive of negative response biases and
lower approach behavior among children playing confines especially with the benefit of digital
a videogame task with peer confederates. technology (Glenn et al., 2019; Le & Beidel,
2017).
ocial Phobia and Anxiety Inventory

S Peer Report
for Children (SPAI-C; Beidel et al., Peer nominations or ratings of social status may
1995) be particularly useful in gauging the generaliza-
tion of treatment effects. Classic sociometric
The SPAI-C consists of 26 multi-part items nomination procedures categorize children along
assessing overt behavior, thoughts, and physio- two dimensions: social preference (how much a
logic responses across a range of potentially fear- child is liked or disliked by his or her peers) and
inducing situations. Beidel, Turner, Hamlin, and social impact (the child’s visibility within the
Morris (2000) have provided data on the external peer group; Coie et al., 1982). Due to the effort
and discriminant validity of the measure. The required to obtain peer reports within school set-
SPAI-C has been shown to correlate with inde- tings, such data typically are included only in the
pendent observer ratings of anxiety and effective- context of extended research investigations and
ness during behavioral performance tasks, as seldom systematically collected by clinicians
well as with children’s ratings of their own anxi- engaged in routine treatment.
ety and distress. Importantly, the measure suc-
cessfully discriminates between children with
SAD, normal controls, and those with other anxi- Psychological Treatment of Social
ety disorders (Viana et al., 2008). Psychometric Anxiety
properties of the SPAI-C also have been estab-
lished with cross-cultural samples (Aune et al., Theoretical Models Underlying
2008; Pina et al., 2014; Scaini et al., 2012), and a Behavioral and Cognitive-Behavioral
validated brief version of the SPAI-C is also Treatment
available (Bunnell et al., 2015).
Several investigations have examined the Current empirically supported treatments for
association of the SPAI-C and SASC-R and have social anxiety have their roots in the historical
found that the measures appear to assess overlap- work on classical conditioning and operant learn-
ping, but not identical constructs (Morris & ing conducted by John Watson and B.F. Skinner.
Masia, 1998; Epkins, 2002). General findings Watson’s case study of “Little Albert” (Watson &
have been that the SPAI-C has greater specificity Rayner, 1920) illustrated how fear and anxiety
and selectivity for diagnoses of SAD. However, may develop through the pairing of aversive and
as the SASC-R typically takes less time to admin- neutral stimuli, which may then rapidly extend to
ister than the SPAI-C, the SASC-R may be pref- other associated stimuli. Accordingly, the classi-
erable in large-scale screening investigations. cal conditioning paradigm has been put forth as
one explanation for the acquisition and general-
Behavioral Observation ization of the heightened physiological arousal
and Performance Tasks experienced by children with anxiety disorders.
Direct observation of behavior is a critical com- In his work on operant conditioning, Skinner
ponent of the assessment of social anxiety and emphasized that behavior is learned as a function
associated social skills. Observation of children of its consequences (Skinner, 1953). Anxiety-
in the natural setting (e.g., school classroom or related responding (e.g., avoidance) will increase
on the playground during recess) may be particu- if followed by a pleasurable event (positive rein-
larly enlightening if one is able to move beyond forcement) or the removal of an aversive stimulus
clinic walls. However, relevant analog or role- (negative reinforcement). All children experience
play tasks may readily be conducted within office normal, developmentally appropriate fears which
are relatively limited and decrease over time negative evaluation and embarrassment (e.g.,
(King, Muris, & Ollendick, 2005). Young chil- “What if I mess up and they all laugh at me?”).
dren may whine, cry, or engage in oppositional While at first glance behavioral and cognitive
behavior in an attempt to escape or avoid a feared perspectives on the development and mainte-
stimulus or situation. By comforting their dis- nance of anxiety disorders may appear in con-
tressed child, parents may inadvertently reinforce flict, many contemporary theorists have noted
inappropriate fearful or avoidant behavior, which that it is not necessary to treat cognitions as a dis-
increases the likelihood of the child responding tinct class in that the same principles of learning
in a fearful and avoidant way in the future. In the apply to cognitions as to physiological and overt
case of social anxiety, parents who allow their behavioral responding. The more relevant ques-
child to refuse to participate in social activities tion really lies with which approach to treatment
with same-age peers, or to stay home from school will be most effective for which individuals. As
in order to avoid the distress of an oral spelling such, it is important to consider the specific
bee, are strengthening the child’s avoidance mechanisms which make SAD treatments
behavior and reducing the chance of learning that effective.
the feared event is not as bad as anticipated.
Clearly, both classical and respondent
approaches have a place in furthering our under- Behavioral and Cognitive-
standing of anxiety. Mowrer (1947, 1960) pro- Behavioral Treatment Components
posed a two-factor learning theory that serves to
integrate the two paradigms. To summarize, upon Behavioral and cognitive-behavioral approaches
exposure to an aversive event, the child responds to the treatment of social anxiety in children and
with increased physiological reactivity and sub- adolescents have received strong empirical sup-
jective distress. This uncomfortable physiologi- port (Scaini et al., 2016). As most treatment pro-
cal arousal then becomes associated with grams have included one or more of the following
previously neutral stimuli present at the time components, these frequently implemented tech-
(including external environmental stimuli and niques will be covered briefly before the research
internal cognitive cues that may serve as remind- findings from specific treatment packages are
ers of the aversive event). As this state of height- reviewed.
ened physiological arousal is aversive for the
child, escape from associated stimuli is nega-
tively reinforced through reduction of arousal— Exposure Therapy
increasing the likelihood of subsequent avoidance
behavior. In a vicious cycle, extended avoidance Ample empirical evidence suggests that exposure
further reduces the likelihood that the child will may be the key component in the successful
develop the necessary skills to manage arousal treatment of child anxiety disorders (Ale et al.,
and anxiety in the future. 2015; Peris et al., 2015; Whiteside et al., 2015).
Following the early behavioral work on condi- Exposure involves having the child face the
tioning and learning, later theorists such as Albert feared stimulus or situation for a sufficient period
Ellis and Aaron Beck sought to provide more of time for anxious physiological arousal to
focus on cognitive factors underlying anxiety. habituate or diminish. The repeated presentation
The basic premise of most cognitive models is of feared stimuli (e.g., public speaking) followed
that anxiety stems from a response bias in which by the absence of the feared consequence (e.g.,
an individual overestimates the probability of being laughed at) teaches the child to associate
threat in their environment and underestimates the stimuli with a neutral or even positive
their ability to cope with the situation (Ellis & response (Craske et al., 2014).
Harper, 1975; Beck, 1976). Children with social Exposure-based techniques include flooding,
anxiety may engage in self-talk emphasizing graduated exposure, and systematic desensitiza-
tion. Flooding involves sustained exposure to afternoon. In addition, if Brennan tries to avoid
attending school on any day, he will forfeit his
highly feared stimuli (in vivo or imaginally), allotted television time for 2 days.
whereas graduated exposure refers to progressive
exposure to feared stimuli proceeding from less Contingency management contracts can be par-
feared to more feared. While flooding has been ticularly useful in providing a system of rein-
used to great success in the treatment of OCD forcement for the completion of between-session
and PTSD, it is less frequently employed in the homework assignments employed in conjunction
treatment of social anxiety in children and ado- with graduated exposure treatment plans.
lescents—in part due to the generalized complex-
ity of social stimuli central to social anxiety and
to the perception that graduated exposure is eas- Social Skills Training
ier to tolerate, which increases willingness to
engage in treatment. Due to its efficacy and rela- Social skills deficits are commonly implicated in
tive ease of administration, graduated exposure the presentation of social anxiety in children and
has become a standard component of many treat- adolescents (Beidel et al., 1999; Halls et al.,
ment protocols for social anxiety. 2015). Children who manifest extreme shyness
In contrast to flooding and graduated exposure and social avoidance from an early age may miss
techniques, systematic desensitization requires out on opportunities to learn age-appropriate
that the child first master relaxation training. social skills. Real or perceived social skills defi-
Once the child is in a relaxed state, the therapist cits may then lead to heightened anxiety in social
presents items from the child’s fear hierarchy. situations. Social skills training (SST) programs
There is no strong empirical evidence to suggest generally include coaching, modeling, and social
that the inclusion of relaxation training yields any problem-solving components. Common skills
incremental gain to the success of exposure in the covered in such programs include peer group
treatment of social anxiety, and some theorists entry and exit strategies, conversational skills,
would contend that use of relaxation or distrac- assertiveness, and developing and maintaining
tion strategies may impede the process of extinc- friendships. SST may even be more effective than
tion. However, some therapists may find that the exposure therapy for treating SAD (Beidel et al.,
process of relaxation training helps establish rap- 2014). The research suggests that children with
port which in turn may foster cooperation among SAD behave in less socially acceptable ways
extremely fearful children during subsequent than children with generalized anxiety disorder
exposure sessions. which could explain why cognitive-behavioral
treatments alone are not as effective as SST in
treating SAD (Scharfstein & Beidel, 2011;
Contingency Management Scharfstein & Beidel, 2015). SST components
have been included in several of the empirically
Contingency management entails the provision supported treatments for social anxiety discussed
of specific consequences for the child engaging later in this chapter.
in specific target behaviors. This typically
involves working closely with the child’s parents
(and possibly teachers) to develop contracts out- Peer Modeling and Peer-Pairing
lining the manner in which rewards and punish-
ment will be delivered for the performance or Peer relationships are central to social and emo-
absence of specific behaviors. For example, a tional development. Interaction with peers pro-
contract targeting social interaction may state: vides a crucial context for the learning of social
If Brennan joins a group activity with his peers skills and emotion regulation. Children who are
during recess on three of five school days, the fam- isolated from their peers are at increased risk for
ily will go to a movie of his choice on Saturday chronic social anxiety and other forms of psycho-
pathology. Consequently, the incorporation of behavioral performance tasks) perhaps because

peers in the treatment of social anxiety may be socially anxious children believe their social
very beneficial. Peer-helper interventions involve skills are worse than they are (Cartwright-Hatton
the selection and training of socially skilled peers et al., 2005; Parr & Cartwright-Hatton, 2009).
who model desired social behavior and adminis-
ter reinforcement to the target child. In contrast,
peer-pairing interventions merely provide strate- Multi-component Programs
gic opportunities for the target child to engage in for the Treatment of Social Anxiety
joint activities with a more socially skilled peer
(with no formal training required of the peer). While there is a strong literature supporting
One advantage of peer-pairing is that it is rela- behavioral therapy and cognitive- behavioral
tively easy to implement within activities occur- therapy for treating SAD in children, the limita-
ring in the child’s natural environment, thus tions of such therapies have led to utilization of
allowing for enhanced generalization. Notably, adapted treatments such as group therapy, social
simple peer-pairing interventions have been skills training, school-based approaches, and
shown to increase positive social interaction and parent-based approaches (Scharfstein & Beidel,
sociometric status among peers (Morris et al., 2011). These adaptations are receiving increased
1995). research support as it becomes clearer that the
treatment for SAD may differ in unique ways
from the treatment for other childhood anxiety
Cognitive Restructuring disorders (Scharfstein & Beidel, 2011).
The term cognitive restructuring encompasses a

variety of techniques intended to alter maladap- Cognitive-Behavioral Group
tive thinking patterns, increase the frequency of Treatment for Adolescents (CBGT-A)
positive self-talk, and enhance self-concept.
Cognitive restructuring techniques require that CBGT-A initially was designed as a 16-week
the client have sufficient metacognitive and logi- treatment program consisting of psychoeduca-
cal reasoning skills to engage in formal problem- tion, skill building, cognitive restructuring, and
solving. As such, cognitive restructuring exposure to socially distressing or fearful situa-
techniques are not likely to be effective with very tions (Albano et al., 1995). Hayward et al. (2000)
young children. In the treatment of adolescents conducted a study in which 35 adolescent girls
with social anxiety, cognitive restructuring is were assigned to CBGT-A or waitlist control
often employed to target irrational self-statements conditions. Significantly fewer adolescents in the
tied to fear of negative evaluation (“I’m nobody. I treatment condition met diagnostic criteria for
want to ask Dylan to the prom but I know she will social phobia following intervention. However,
say no…then everyone will make fun of me... no differences between groups were found at
and no one will ever go out with me”). one-year follow-up.
Cognitive restructuring is typically combined Herbert and colleagues (Herbert et al., 2009)
with modeling and reinforced practice, and as have reported results from a randomized con-
such is rarely implemented as a purely cognitive trolled trial comparing three forms of treatment:
procedure. Empirical findings have been mixed (a) a 12-week group treatment program (G-CBT)
regarding the incremental utility of using expo- reported as similar to that of CBGT-A, (b) indi-
sure and cognitive restructuring in combination. vidual CBT, and (c) group psychoeducational
With respect to treatment outcome, the benefits supportive therapy. Large effect sizes were
of cognitive restructuring tend to be more pro- yielded for all three treatments. Treatment condi-
nounced for self-report data than for direct mea- tion was not related to symptom reduction as
sures of behavioral change (e.g., observation and measured by self-reports (SPAI-C, SAS-C) or
clinician severity ratings (CGI-S). At treatment compared to only 5% of those receiving the
completion, there were no significant group active control treatment.
differences on treatment responder criteria (with Extensive follow-up data have been reported
recovery rates of 16–29%). However, at the three- for SET-C. Beidel et al. (2005) provided results
month follow-up assessment, greater treatment of a three-year follow-up assessment that
response (54%) was observed for adolescents included 90% of children who completed the
who completed the course of G-CBT. Significant original controlled trial of SET-C. Seventy-two
limitations of the study include the relatively percent of these children (now aged 11–18) no
small initial sample size (23–26 per group), a longer met criteria for SAD, a significant increase
29% treatment drop-out rate, and further attrition from the 62% who were diagnosis-free at the end
of 27% for the final assessment (follow-up data of treatment. No participants had sought addi-
were obtained for only 13 adolescents in the tional intervention following the completion of
G-CBT group). SET-C, thereby supporting the durability of treat-
ment gains. At five-year follow-up, 25 SET-C
completers (now aged 13–20) were reassessed
Social Effectiveness Therapy and compared to a matched non-clinical sample
for Children (SET-C) to determine long-term treatment effects (Beidel
et al., 2006). None of the individuals had sought
Beidel, Turner, and Morris (2000) published the pharmacological or psychological treatment after
first randomized controlled trial of behavioral completing SET-C, yet 80% no longer met crite-
treatment for social phobia in pre-adolescent ria for SAD (a recovery rate that continued to
children. In contrast to “cognitive-behavioral” climb from post-treatment through extended fol-
treatment programs such as CBGT-A, SET-C low-up). Comparing treatment responders to the
does not include a cognitive restructuring com- matched non-clinical controls, there were no dif-
ponent. SET-C is a 12-week behavioral inter- ferences in self-report, parent report, or observa-
vention that incorporates parent education, tion of social skill—thus demonstrating
group social skills training, peer generalization, meaningful and lasting change for these formerly
and individual graduated in vivo exposure com- socially anxious children. Another follow-up
ponents. Instruction, modeling, behavior study found that child-reported loneliness medi-
rehearsal, feedback, and social reinforcement ated the improvement in social anxiety symptoms
are used to teach and reinforce appropriate (Alfano et al., 2009).
social behavior. A unique and essential compo- Baer and Garland (2005) conducted a pilot
nent of SET-C is the use of peer interaction investigation in which they substantially modi-
experiences (age-appropriate group recreational fied the SET-C protocol to create a simplified
activities with peer facilitators) to assist in the treatment for use in community psychiatric clin-
generalization of social skills to situations out- ics by encouraging participants to find peer or
side the clinic. Fifty children (aged 8–12) were family “coaches” who could help with exposure
randomized to SET-C or an active treatment for practice in the natural environment. Following
improving test taking and study skills. Children intervention, 36% of adolescents in the treatment
in the SET-C group demonstrated statistically group no longer qualified for a diagnosis of social
and clinically significant improvements across phobia, while no members of the waitlist group
multiple domains (including self-reported anxi- demonstrated such improvement. Although
ety, independently observed social skills, and reported effect sizes were smaller than those
adaptive functioning in daily situations), and obtained with the SET-C, the authors note that
gains were maintained 6 months post-treatment. this modified treatment may be more easily trans-
Notably, 67% of children who participated in ported to community settings. Another pilot
the SET-C program no longer met diagnostic study reported the feasibility of an adaption of
criteria for social phobia following treatment the SET-C using virtual environment technology
in order to increase practice opportunities and of anxious behavior, including parents in the
generalizability of the context and found that treatment process may be prudent. Spence et al.
(Wong Sarver et al., 2014). (2000) investigated the effectiveness of a
cognitive-behavioral treatment (CBT) program
with or without parental involvement. Fifty chil-
School-Based Intervention dren diagnosed with social phobia (aged 7–14)
were randomly assigned to CBT, CBT plus
Programs that take place at school allow better parental involvement (CBT-PI), or a waitlist con-
access to evidence-based care as well as opportu- trol condition. CBT components included social
nities to practice in an ecologically valid context skills training, relaxation, cognitive restructur-
(Masia-Warner et al., 2015). Masia-Warner and ing, and graduated exposure. The parent involve-
colleagues reported results for 42 adolescents ment component was designed to help parents
with SAD who were randomized within their model and reinforce the social skills taught in
schools to Skills for Academic and Social Success CBT, ignore anxious and avoidant behavior,
(SASS) or a waitlist control condition (Masia- encourage their child’s participation in social
Warner et al., 2005). SASS, based in part on the activities, and provide contingencies for home-
SET-C and CBGT-A programs, consisted of 12 work completion. Parents participated in a
in-school sessions including psychoeducation, 30-minute weekly training session and also
cognitive restructuring, social skills training, observed the children’s group sessions behind a
exposure, and relapse prevention; two individual one-way mirror. The CBT and CBT-PI interven-
problem-solving meetings; four unstructured tions both included 12 weekly group sessions and
social events; two psychoeducational parent 2 booster sessions (at 3 months and 6 months
meetings; and two brief psychoeducational post-treatment). Based on parent report, children
teacher meetings. At treatment completion, 67% in both active treatment groups demonstrated
of adolescents completing SASS no longer met improvement in social skills. However, statisti-
the criteria for SAD, compared with only 6% in cally significant differences were not found for
the waitlist control condition. either treatment with respect to children’s total
In further work with the SASS (Masia-Warner number of peer interactions or independent
et al., 2007), 36 adolescents diagnosed with SAD observer ratings of assertiveness. While CBT and
were randomized to 12 weeks of SASS or an CBT-PI both resulted in a decrease in social anxi-
attention-control condition termed Educational- ety symptoms, neither yielded statistically sig-
Supportive Group Function (ESGF). ESGF nificant change in social behavior, thus perhaps
included psychoeducation and general relaxation providing support for the inclusion of peers in an
skills but did not include social skills training, effort to enhance generalization to the child’s
cognitive restructuring, exposure, or peer gener- natural social environment. There also is evi-
alization components. SASS proved superior to dence to support the utility of stand-alone, parent-
ESGF (59% versus 0% diagnosis-free) with based treatment for childhood anxiety disorders
symptom improvement maintained at a six- (Lebowitz et al., 2020). Supporting Parenting for
month follow-up. Anxious Childhood Emotions (SPACE) involves
working with parents to reduce parental accom-
modation and validate their child’s anxious feel-
ognitive-Behavioral Treatment Plus
C ings while expressing their confidence in their
Parental Involvement child’s ability to tolerate distressing situations.
SPACE was shown to be non-inferior to child-
Given the mounting evidence that parents may only CBT (versus family-based) for anxiety out-
play a role in the development and maintenance comes (including social anxiety) in children.
Pharmacological Treatment ment on self-report and parent-report measures.

of Social Anxiety Another open-label pilot trial used the antide-
pressant mirtazapine (Remeron) with 18 children
At present, the most widely prescribed pharma- and adolescents diagnosed with SAD (Mrakotsky
cologic agents for the treatment of social anxiety et al., 2008). A significant decrease in social anx-
in children and adolescents are the class of drugs iety symptom severity and impairment was
known as selective serotonin reuptake inhibitors observed after 8 weeks of treatment. However,
(SSRIs). Serotonin-norepinephrine reuptake notable weight gain was observed (M = 3.27 kg)
inhibitors (SNRIs) such as venlafaxine and and four participants experienced additional side
duloxetine have some support in treating children effects (e.g., moderate sleepiness, moderate
with SAD (March et al., 2007). On the other headaches, and increased depressive symptoms).
hand, no randomized control trial to date has The antidepressant tandospirone was tested in an
found tricyclic antidepressants, buspirone, or open-label controlled trial in children with social
benzodiazepines clearly effective for treating anxiety disorder (Huang et al., 2013). The study
SAD in children (Snir et al., 2021). We report found that 48.6% of children taking tandospirone
below studies that focused only on youth with showed clinical global improvement as compared
social anxiety (versus studies who sampled youth to 55.6% of children taking sertraline.
with a variety of anxiety presentations).
The SSRI paroxetine (Paxil) was tested in a
large multicenter randomized placebo-controlled Comparison of CBT
trial of 322 children and adolescents with SAD and Pharmacologic Treatments
(aged 8–17; Wagner et al., 2004). Following
16 weeks of treatment, clinician-rated improve- Segool and Carlson (2008) present the results of
ment was significantly greater for paroxetine a meta-analysis in which they reviewed seven
(48%) than placebo (15%). Adverse side effects CBT trials and seven SSRI trials conducted
were relatively infrequent and included insomnia between 1994 and 2004 for children and adoles-
(14.1% vs. 5.8%), decreased appetite (8.0% vs. cents (aged 6–19) with SAD. All evaluated CBT
3.2%), and vomiting (6.7% vs. 1.9%). The SNRI studies included cognitive restructuring and
venlafaxine (Effexor) was tested against placebo exposure, and the majority included psychoedu-
in a randomized controlled trial of 293 children cation and social skill training components. It
and adolescents with SAD (aged 8–17) who were should be noted that the authors excluded results
treated across 48 academic and community clin- from SET-C trials on the basis that SET-C is a
ics (March et al., 2007). Drop-out rate was 35% behavioral intervention that does not include cog-
for venlafaxine versus 27% for placebo control. nitive restructuring. Studies ranged in duration
After 16 weeks, treatment response to venlafax- from 3 weeks to 16 weeks. All CBT and SSRI
ine was significantly larger than placebo as deter- treatments yielded moderate to large effect sizes
mined by self-report (SAS-C/A) and clinician (0.59–2.92) for reduction of social anxiety symp-
ratings (CGI-Improvement). Notably, there were toms and overall impairment, with slightly larger
three reported cases of treatment-emergent sui- effects for SSRIs. Gains in social competence
cidal ideation in the venlafaxine condition, with were somewhat (but not significantly) higher for
none occurring in the placebo condition. CBT than SSRI. The authors noted major limita-
In addition, several open-label studies have tions in drawing conclusions across studies, in
been conducted for children with SAD. The SSRI part due to the lack of universally applied assess-
escitalopram (Lexapro) was used to treat 20 chil- ment measures.
dren and adolescents with social anxiety disorder As the Segool and Carlson meta-analysis
(Isolan et al., 2007). After 12 weeks of treatment, excluded SET-C, it is important to note the find-
65% of the intent-to-treat sample met treatment ings of research directly comparing SET-C with
response criteria and showed significant improve- SSRI treatment. Children and adolescents with
SAD (aged 7–17) were randomized to 12 weeks behavioral treatment (SET-C) demonstrated dif-
of pill placebo, fluoxetine (Prozac), or SET-C ferential superiority for the behavioral interven-
(Beidel et al., 2007). Participants in the placebo tion. More research is needed on the use of
and fluoxetine conditions attended a 60-minute combined behavioral and pharmacologic treat-
weekly medication management and supportive ment. The literature is rapidly expanding with
counseling session by a psychiatrist. Following respect to our knowledge of potential risk factors
treatment, significantly more participants in the in the development of anxiety (particularly in
SET-C condition met treatment responder criteria terms of parenting), and this information is fur-
and no longer carried a diagnosis of SAD than thering the development of treatment targets and
those in the fluoxetine or placebo conditions. applications. The inclusion of parents and peers
Treatment gains were maintained at one-year in the provision of treatment is an especially
follow-up. In addition, while both SET-C and exciting trend as it reflects increasing develop-
fluoxetine were more effective than placebo at mental sensitivity to the social world of children
reducing social distress and behavioral avoid- and adolescents. As social anxiety is a relatively
ance, only SET-C led to significant improve- early onset and chronic condition, future efforts
ments in social skill and social competence. This should be directed toward early intervention
finding reinforces the idea that social skills are as studies and dissemination of treatments beyond
or more important than anxiety reduction in treat- specialized academic centers. No doubt, front-
ing SAD (Scharfstein et al., 2011). line clinicians will have much to offer as we work
Although the empirical research base primar- toward cost-effective treatments that may be
ily has investigated the use of psychological or delivered through school, home, and clinic set-
pharmacologic treatments in isolation from one tings to the large numbers of children and adoles-
another, clinicians and healthcare providers have cents who are currently underserved.
long stressed the notion that pharmacologic treat-
ments will be enhanced if behavioral or cognitive- Acknowledgments We wish to acknowledge the contri-
behavioral treatments are implemented in butions of Chelsea Ale on a prior version of this chapter.
conjunction (Chavira & Stein, 2002). Medication
may reduce the physiological arousal that accom-
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Treatment of Pediatric
Post-traumatic Stress Disorder 21
Elissa J. Brown, Komal Sharma-Patel,
Kaitlin Happer, and Amy Hyoeun Lee
Trauma is defined as exposure to threatened or 2019), defined as including the criteria for PTSD
actual death, serious injury, or sexual violence plus difficulties with affect regulation, self-
(American Psychiatric Association, 2013). Based concept, and relationships with others. For chil-
on national surveys of adolescents, more than dren exposed to trauma, approximately 50% have
60% of children in the United States are exposed at least one symptom of PTSD and 20% meet full
to trauma prior to age 18 (e.g., Finkelhor et al., criteria for the disorder (e.g., Alisic et al., 2014).
2015). Post-traumatic stress disorder (PTSD) is These findings underscore the need for inter-
the most common sequelae to trauma. In the vention for preschoolers, children, and adoles-
Diagnostic and Statistical Manual of Mental cents who have been exposed to trauma. This
Disorders, fifth edition (2013), the APA charac- chapter examines treatment outcome studies of
terizes PTSD by symptoms of intrusion (e.g., psychosocial treatments for PTSD in youth. The
nightmares, flashbacks), avoidance (e.g., of following sections include theoretical and practi-
thoughts, feelings, places, or people that are cal arguments for cognitive-behavioral therapy
reminders), negative changes in cognition and (CBT), the psychosocial intervention with the
mood (e.g., self-blame, anhedonia), and hyper- most scientific support. Specific treatment con-
arousal (e.g., exaggerated startle response, hyper- siderations, including developmental and cultural
vigilance). Symptoms must last for at least 1 factors, are discussed. Lastly, factors related to
month and be associated with functional impair- treatment outcome also are highlighted. In sum,
ment. Complex PTSD is now included in the 11th trauma-specific CBT is well established for pedi-
revision of the International Classification of atric PTSD, and the next step in the field is ade-
Diseases (ICD-11; World Health Organization, quate dissemination and implementation of best
practices.
E. J. Brown (*)
St. John’s University, Jamaica, NY, USA
e-mail: browne@stjohns.edu hild and Adolescent Models
C
K. Sharma-Patel of PTSD Development
Children’s National Medical Center, Washington,
DC, USA Early theoretical explanations of PTSD relied
K. Happer upon classical and operant conditioning learning
Department of Child & Adolescent Psychiatry, NYU paradigms. In brief, traumatic events were concep-
Langone Health, New York, NY, USA
tualized as unconditioned stimuli evoking uncon-
A. H. Lee ditioned responses (e.g., fear), resulting in
Stony Brook University, Stony Brook, NY, USA
https://doi.org/10.1007/978-3-031-14080-8_21
316 E. J. Brown et al.
conditioned pairing between trauma cues (e.g., ous”). Mitchell et al. (2017) found support for
memories, triggers/cues) and re-experiencing this model in children. In addition, amelioration
symptoms (e.g., nightmares, flashbacks). of trauma-specific beliefs in psychosocial treat-
Subsequent models of PTSD have integrated these ment is predictive of improvements of PTSD
conditioning paradigms with research on emotion, (Pfeiffer et al., 2017; Sharma-Patel & Brown,
memory, social-cognition, and neurobiology to 2016).
better explain the structure and persistence of
PTSD symptoms among adults and children.
Emotional processing theory (Foa & Kozak, Using Trauma-Specific Cognitive-
1986, Foa et al., 1989) primarily focuses on the Behavioral Therapy to Treat PTSD
development of maladaptive emotional (i.e., in Youth
excessive fear response to triggers) responses
that underlie anxiety disorders. Briefly, Foa and Description of Trauma-Specific
Kozak (1986) argue that traumatized individuals Cognitive-Behavioral Therapy
have pathological fear structures (i.e., fragmented
memories) that encompass event-related Trauma-specific CBTs are designed to amelio-
unthreatening stimuli (e.g., environmental trig- rate PTSD symptoms in youth in a developmen-
gers), responses (re-experiencing symptoms, tal and cultural framework. Trauma-specific
exaggerated startle response, and hypervigi- CBTs include components that address trauma
lance), and cognitions related to perceived dan- reminders (i.e., re-experiencing symptoms),
ger that serve to maintain avoidance behaviors, avoidance, trauma-specific cognitions, physio-
and thereby, contribute to the development of logical dysregulation, and caregiver factors.
PTSD symptoms. For example, a teen who was Treatment typically begins with psychoeducation
sexually abused by her stepfather, an extermina- of the child and caregiver about the trauma(s)
tor who used a lot of cologne, experienced flash- experienced (e.g., legal terms, prevalence), bio-
backs and physiological symptoms when she psychosocial impact of trauma (focusing on the
smelled over-the-counter pest sprays and men’s child’s specific trauma responses), connections
cologne, and therefore avoided trauma reminders between the child’s trauma and responses, and
(e.g., men wearing cologne, drug store aisles). explanation of how treatment will address these
A related phenomenology of PTSD focuses responses to instill hope for recovery.
on cognitive processing (e.g., self-blame). Affect identification and modulation are used
According to cognitive theories of adverse events, to teach children and caregivers how to identify
PTSD symptoms develop and persist from an and cope with trauma-related emotions of anxi-
incongruity between preexisting beliefs (e.g., ety, anger, sadness, guilt, shame, etc. Children
“There is a just world”) versus attributions about and caregivers learn to recognize and monitor
the traumatic experiences (e.g., Ehlers & Clark, their emotions. Relaxation strategies (e.g., dia-
2000). Trauma survivors with PTSD engage in phragmatic breathing, progressive muscle relax-
assimilation (making the trauma fit into the pre- ation, journaling, mindfulness) are used to
existing belief, which can result in self-blame) or decrease hyperarousal. Skills are presented with
over-accommodation (changing the preexisting psychoeducation on the rationale and steps, then
belief in an extreme way; e.g., “Men can’t be practiced in session and at home.
trusted”). Michael et al. (2007) argue that PTSD Exposure therapy (conducted gradually or via
is a result of cognitions of perceived threat and flooding) and cognitive restructuring are the core
lack of control, maladaptive coping strategies elements of trauma-specific CBT. Cognitive cop-
(rumination, avoidance) and global “trauma- ing is used to address negative thoughts related to
sensitive” beliefs about the self (“There is some- daily life stressors and to challenge the maladap-
thing wrong with me”), others (“I cannot trust tive trauma-specific automatic thoughts that
people”), and the world (“The world is danger- emerge during exposure. Skills include cognitive
21 Treatment of Pediatric Post-traumatic Stress Disorder 317
restructuring, guided visualization, and positive cial treatments for pediatric PTSD. They
self-talk. Exposure to the traumatic memory and included 32 studies with 2260 participants.
associated fear network alters the memory such Results suggested a large positive effect for
that threat cues are re-evaluated in the absence of trauma-specific CBTs delivered individually
aversive consequences (Foa et al., 1989). This is with conjoint parent training. Treatment compo-
conducted through imaginal exposure (also nents found to be efficacious include: cognitive
called trauma narration) in which details of the therapy, somatic interventions (e.g., relaxation),
trauma, and associated feelings and thoughts, are meditation, imaginal and in vivo exposure, and
processed in session. Additional emotions (e.g., family therapy. Treatment packages with the
shame, guilt) are addressed through direct con- strongest evidence were Trauma-Focused
frontation of inaccurate thoughts (i.e., cognitive Cognitive Behavioral Treatment (TF-CBT;
restructuring; Resick & Schnicke, 1992). This Cohen & Mannarino, 1996), Cognitive
discussion of the trauma also allows for elabora- Behavioral Intervention for Trauma in Schools
tion and integration of a clearer memory into the (Jaycox et al., 2012), and Child-Parent
child’s existing memory system (Ehlers & Clark, Psychotherapy (Lieberman et al., 2005). The
2000). For children who are avoiding innocuous authors concluded that TF-CBT, particularly
cues, therapists implement in vivo exposure when implemented as individual therapy with
using a hierarchy of feared situations. Parent conjoint parent training, appears to be most
involvement is used to support participation in effective in the management of PTSD in youth.
and responses to exposure and cognitive restruc- Gutermann et al. (2017) conducted a meta-
turing, as well as manage trauma-related behav- analysis of the long-term treatment effects of
ior problems (Cohen et al., 2000). Peterman et al. psychosocial interventions for pediatric PTSD.
(2015) outline fundamental principles to guide They found that the mean follow-up effect sizes
the use of exposure in children. ranged from medium (for controlled studies) to
In trauma-specific CBT, caregivers participate large (for uncontrolled studies and pooled analy-
for two reasons: (1) to learn to manage their own sis including all studies). These effect sizes were
affect and (2) to coach and support their children. equivalent to those at post-treatment, suggesting
Parent training is incorporated in trauma-specific that treatment effects remain stable at follow-up.
CBT to address the externalizing behavior prob-
lems commonly seen in child trauma survivors.
Throughout coping and exposure phases of sing Other Short-Term
U
trauma-specific CBT, therapists meet with chil- Interventions to Treat PTSD in Youth
dren and caregivers together to practice coping
skills and parenting techniques and plan for home ye Movement Desensitization
E
practice. After completing the trauma narration, and Reprocessing
conjoint child-caregiver sessions are used to
allow the child to share the narrative with the Eye Movement Desensitization and Reprocessing
caregiver, enhance communication between the (EMDR) is described by the developers as a
child and caregiver, and guide the child and care- structured “comprehensive, integrative” therapy
giver in family safety planning and problem- that includes elements from “psychodynamic,
solving prior to termination. cognitive behavioral, interpersonal, experiential
and body-centered therapies” (EMDR Institute,
Inc., 2004). EMDR consists of graduated imagi-
fficacy of Trauma-Specific Cognitive-
E nal exposure sessions with simultaneous visual
Behavioral Therapy tracking of therapist hand movements; however,
there is considerable debate on the mechanisms
In a recent systematic review and meta-analysis, underlying the effectiveness of EMDR (e.g., Lee
Mavranezouli et al. (2020) evaluated psychoso- et al., 2006).
Recent studies have compared EMDR with among diverse groups and settings. The literature
trauma-specific CBT. In a meta-analysis of is reviewed below in the context of these issues.
EMDR versus CBT for children with PTSD
(Moreno-Alcázar et al., 2017), the researchers
found that EMDR was more efficacious than ritical Issues in Treating PTSD
C
waitlist and placebo conditions and similar in in Youth
efficacy to CBT. Similarly, a recent study
(Jaberghaderi et al., 2019) compared TF-CBT, Developmental Considerations
EMDR, and a control condition with children
exposed to domestic violence. They found that Most studies of treatment for PTSD in children
the TF-CBT and EMDR had greater reductions in focus on elementary-school-age and preadoles-
PTSD than the control condition, but there were cent youth. There are important differences in
no differences between the active treatments. clinical presentation of PTSD at different devel-
According to the meta-analysis conducted by opmental levels that should inform treatment
Mavranezouli et al. (2020), EMDR is an effective (Danielson et al., 2010; Scheeringa et al., 2011).
treatment but to a lesser extent than trauma- For example, young children may present with
specific CBT. nightmares that are neither necessarily distress-
ing nor associated with trauma, repetitive play,
and behavior problems. Avoidance symptoms
Psychodynamic Psychotherapy might manifest as age-specific fears (e.g., dark,
monsters, closets). In contrast, adolescents pres-
There is limited research suggesting the efficacy ent with risky behaviors (e.g., substance abuse)
of psychodynamic psychotherapy for pediatric and are more likely to report numbing. Below is
PTSD. Parker and Turner (2014) conducted a a summary of treatment studies conducted with
systematic review of psychodynamic psychother- preschoolers and adolescents, with associated
apy for sexually abused children. They conducted clinical recommendations.
a thorough search for randomized and quasi-
experimental designs comparing psychodynamic Treatment of preschoolers Two early trials of
psychotherapy to treatment-as-usual or waitlist TF-CBT with preschoolers with PTSD secondary
conditions. They found no studies that met their to sexual abuse showed promising outcomes
inclusion criteria. (Cohen & Mannarino, 1996; Deblinger et al.,
2001). More recently, Hébert and Daignault
(2015) conducted a pilot study of TF-CBT with
Summary of Psychosocial sexually abused preschoolers and found reduc-
Treatments for PTSD tions in PTSD, with gains maintained at 1-year
follow-up. In a study of preschoolers with vary-
In sum, trauma-specific CBT and EMDR are effi- ing trauma histories, Scheeringa et al. (2011)
cacious for pediatric PTSD. TF-CBT has the found that not only did TF-CBT participants evi-
strongest empirical support, with more than 20 dence significantly greater reductions in PTSD
randomized controlled trials supporting its effi- symptoms compared to the waitlist condition,
cacy. Access to TF-CBT has been made easier by preschoolers in TF-CBT were able to compre-
the web training (https://tfcbt2.musc.edu), Train- hend and complete over 80% of the treatment
the-Trainer program, and evidence of its efficacy content. Similarly, Salloum et al. (2014) found
via telehealth (Stewart, Orengo-Aguayo, Young, support for the use of TF-CBT provided in a
et al., 2020). More research is needed to better stepped care model with preschoolers. The par-
assess and treat developmentally specific trauma ticipants showed reductions in PTSD and main-
sequelae, determine long-term effects of treat- tained gains at a 3-month follow-up. In a pilot
ment, and show effectiveness of these treatments RCT by Salloum et al. (2017), a stepped-care
approach to delivery of TF-CBT (in which care- mainly because most samples in the studies of
givers were trained to deliver treatment compo- TF-CBT have included both children and adoles-
nents) was compared to standard TF-CBT cents. Supplementing these investigations, effec-
(delivered by clinicians) for preschoolers. There tiveness trials solely with adolescents also have
were no differences in outcomes, but the cost of demonstrated comparable findings (Cisler et al.,
stepped care was significantly less than standard 2015; Weiner et al., 2009).
TF-CBT.
In addition, there is an emergence of studies
Pollio and Deblinger (2017) reviewed some of on the treatment of adolescent PTSD and integra-
the modifications that have been made to TF-CBT tive interventions to treat PTSD and co-occurring
for preschoolers including shortened sessions, problems. To date, there has been one random-
focused time on skill building or narration fol- ized trial of adolescents receiving prolonged
lowed by planned positive activities or breaks, exposure (PE; Foa et al., 2013). They found that
and repetition of skills for acquisition. There also sexually abused girls who received PE (versus
is a stronger emphasis on caregiver involvement. supportive counseling) had greater reductions in
For instance, caregivers are provided psychoedu- PTSD and depressive symptoms, with gains
cation on normative transient fears and normative maintained at 12-month follow-up.
noncompliance, with the goal of differentiating The integrative treatments incorporate multi-
from trauma-related problematic behaviors. ple evidence-based approaches in one package,
Relaxation skills are simplified with metaphors often used modularly, to address co-occurring
(e.g., cooked/uncooked spaghetti), visualizing, problems (e.g., PTSD and substance use/risky
and drawing images of calming scenes or situa- sexual behavior). For example, Risk Reduction
tions (e.g., beach, waterfalls). Affect expression through Family Therapy (RRFT; Danielson et al.,
is taught using concrete and play-based activities 2012) integrates TF-CBT into its model along
(e.g., feeling charades). For cognitive skills, sim- with family and community-level interventions.
pler prompts (e.g., what is your brain saying?) Danielson et al. (2012) reported greater improve-
and identifying “unhelpful and helpful” thoughts ments in PTSD symptoms, depression, and sub-
to generate better coping statements are some of stance use risk for teens receiving RRFT (versus
the recommended strategies. Finally, for trauma treatment as usual) in their randomized control
processing, young children may benefit from trial. Seeking Safety (Najavits et al., 2006),
more structure, prompting, and use of creative another integrative treatment with coping skills
arts to facilitate the narration. and modified trauma narration developed for
An evidence-based trauma treatment that was teens with substance abuse and PTSD, has been
developed specifically for young children (ages investigated in a small randomized controlled
birth-5) is Child-Parent Psychotherapy (CPP; trial with results supporting its utility.
Lieberman et al., 2015). CPP focuses on the Two integrated interventions without care-
attachment relationship and, thus, is implemented giver involvement have less successful results.
in a dyadic format with primary caregivers. There Trauma Affect Regulation: A Guide for Education
are five randomized controlled trials demonstrat- and Therapy (TARGET; Ford et al., 2012) is a
ing its efficacy to improve caregiver functioning, skill-based treatment without caregiver involve-
parent-child relationship, and child trauma symp- ment and exposure that has been tested with trau-
toms (Hagan et al., 2017). matized youth in juvenile justice systems, with
mixed findings when compared to other treat-
Treatment of adolescents In the last decade, ments (see Black et al., 2012 for review). Skills
there has been an increase in recognition that Training in Affect Regulation (STAIR; Cloitre
trauma treatment for adolescents warrants par- et al., 2001), an intervention with coping skills
ticular attention. TF-CBT is considered the gold (psychoeducation, behavioral, and cognitive cop-
standard for adolescents (Black et al., 2012) ing skills to address affect and interpersonal
dysregulation) and exposure, originally devel- to waitlist control, supportive psychotherapy, and
oped and found efficacious for adult women with routine community care (Cohen et al., 2018).
sexual abuse histories, has been modified and Deblinger et al. (2011) demonstrated significant
studied in two open trials, applied in a group for- improvements in PTSD symptoms regardless of
mat in schools (Gudiño et al., 2016) and inpatient treatment length (8 versus 16 sessions) with gains
for adolescents (Gudiño et al., 2014) with mixed maintained at a 12-month follow-up (Mannarino
results for PTSD. et al., 2012).
Analogous to developmental modifications
for preschoolers, these treatment approaches
include prescriptions for adolescents (e.g., Black Child Physical Abuse
et al., 2012). Psychoeducation may include infor-
mation about the effects of trauma on specific Decades of evidence demonstrate CBT as an
areas of the brain that can maintain PTSD symp- effective intervention for child physical abuse,
tomatology or influence risky behavior. Coping particularly when parents are included in treat-
skills are often expanded to incorporate mindful- ment. Alternatives for Families: a CBT (AF-CBT;
ness and meditative strategies, and journaling. Kolko, 1996a; Kolko et al., 2011) includes
Given that adolescents often experience chronic offending caregivers in treatment to improve par-
trauma, narration may include a life timeline and enting skills, safety, and family outcomes, in
discussion of themes (e.g., dangerous world) addition to child symptomatology. An early RCT
instead of processing every incident of trauma. (Kolko, 1996b) comparing parent and child CBT
Finally, safety planning often occurs from the and AF-CBT to TAU found that both active treat-
onset of treatment to address risky behavior (e.g., ments led to improvements in children’s internal-
self-injury, substance use). izing and externalizing symptoms and
parenting-related variables. In a nonrandomized
sample of 195 children (ages 5–15 years old),
Trauma Type AF-CBT led to significant reductions in PTSD
symptoms and improvements in family dysfunc-
Trauma type has been shown to be an important tion compared to TAU (Kolko et al., 2018). A
predictor of PTSD with prevalence rates varying similar parent-child CBT intervention (Runyon
from 13% following natural disaster to 35% fol- et al., 2010) has been found to be efficacious in
lowing sexual abuse (Alisic et al., 2014). In turn, decreasing PTSD symptoms (Thulin et al., 2020).
treatment of PTSD may vary based on trauma type. Multisystemic Therapy for Child Abuse and
Although exploration of all trauma types is beyond Neglect (MST-CAN; Swenson et al., 2010), an
the scope of this chapter, below is a summary of intensive, in-home program that treats youth and
research on treatment of PTSD following common caregivers, also showed significant decreases in
trauma types most often studied in the literature. PTSD symptoms compared to standard care in a
sample of 86 physically abused youth (10–
Sexual abuse/assault Research has demon- 17 years old) and families.
strated that CBT, specifically TF-CBT, is effec-
tive for reducing symptoms of PTSD in victims Witnessing domestic violence In a review of
of child sexual abuse. Deblinger et al. (1996) treatments for children who witnessed interper-
evaluated the efficacy of TF-CBT in treating sonal violence, Anderson and Van Ee (2018)
PTSD in a sample of 90 children (7–13 years old) found that programs with parents and children
and their caregivers, with greater reductions in working individually and jointly were most suc-
PTSD symptoms compared to control, main- cessful in addressing pediatric PTSD. An RCT
tained 2 years post-treatment (Deblinger et al., examining TF-CBT among 124 youth (7–14 years
1999). Since this study, TF-CBT has been found old) with histories of witnessing domestic
superior in reducing PTSD symptoms compared violence demonstrated a significant decrease in
PTSD symptoms compared to usual care (Cohen with CBITS and CBITS-plus-family, with addi-
et al., 2011). Jaberghaderi et al. (2019) compared tional improvements in school involvement and
a CBT (based on AF-CBT), EMDR, and a control attitude toward mental health in the family group.
condition in 139 Iranian youth (8–12 years old)
exposed to domestic violence; they found signifi-
cant decreases in PTSD in both treatments com- War
pared to control.
Meta-analyses of war and terrorism exposure
School-based treatments also have been suc- interventions suggest that CBT-based interven-
cessful in treating youth exposed to interpersonal tions are most effective in alleviating PTSD
violence. Cue-centered treatment is a school- (Nocon et al., 2017), particularly with cultural
based manualized treatment to help youth iden- adaptations (e.g., translation of materials; Jordans
tify how trauma impacts current behaviors and et al., 2016). Culturally modified TF-CBT has
emotions, and to use insight-oriented strategies to been shown robust outcomes in Zambia (Murray
respond adaptively to trauma cues. Cue-centered et al., 2013), Kenya (Dorsey et al., 2020), and the
treatment resulted in a greater decrease in PTSD Republic of Congo (McMullen et al., 2013;
compared to waitlist control in an RCT of 65 O’Callaghan et al., 2013). School-based CBT
youth (8–17 years old) exposed to domestic vio- also has been found to be efficacious with war-
lence (Carrion et al., 2013). The Kids’ Club exposed children in Indonesia (Tol et al., 2008),
(Graham-Bermann, 1992), a group focusing on Syria (Gormez et al., 2017), and with Palestinian
emotion identification, coping skills, cognitive youth (Qouta et al., 2012).
restructuring, and safety planning, was effective
in reducing PTSD symptoms in school-aged chil- Disasters A meta-analysis of interventions for
dren (Vickerman & Margolin, 2007) and decreas- youth victims of disasters identified CBT, EMDR,
ing internalizing symptoms in preschool-aged and narrative exposure therapy as having the best
children (Graham-Bermann et al., 2015). outcomes (Brown et al., 2017). CBT also has
been found to be efficacious for PTSD related to
traumatic bereavement following disaster.
Community Violence Brown, Goodman, et al. (2020) conducted an
RCT comparing TF-CBT with Client-Centered
A systematic review of programs for youth Therapy for 40 children-mother dyads who expe-
exposed to community violence (Ali-Saleh rienced the death of the father during 9/11. They
Darawshy et al., 2020) reported an overall dearth found that both treatments led to significant
of well-designed studies in extant literature, with improvements in children’s PTSD, depression,
CBT approaches demonstrating the best evi- and grief symptoms, whereas caregivers receiv-
dence. Cognitive-Behavioral Intervention for ing TF-CBT had greater symptom reduction than
Trauma in Schools (CBITS; Jaycox et al., 2012) those receiving Client-Centered Therapy.
is a school-based intervention using CBT strate-
gies in weekly group sessions, with additional Accessibility and delivery of treatment is an
individual and educational sessions, to address important consideration following large-scale
PTSD, anxiety, and depression in traumatized disasters. In a field trial, Jaycox et al. (2010)
youth. Use of CBITS in an RCT of 126 middle- compared youth with PTSD randomized to
school youth resulted in improvements in PTSD CBITS versus TF-CBT following Hurricane
symptoms, depression, psychosocial dysfunc- Katrina. They found decreases in PTSD in both
tion, and academic performance (Kataoka et al., conditions. There was a slightly larger decrease
2011; Stein et al., 2002). Santiago et al. (2015) for children in TF-CBT, but CBITS was per-
found a significant decrease in PTSD and depres- ceived as more accessible. In a pilot study of an
sive symptoms in 40 parent-child dyads treated adaptation of CBITS that excludes exposure and
allows for nonclinician delivery, Jaycox et al. Villalobos, et al., 2020; Stewart, Orengo-Aguayo,
(2009) found a significant decrease in PTSD Young, et al., 2020).
symptoms in flood-impacted Pakistani youth. For Given the disparities in trauma exposure
easier accessibility, Ruggiero et al. (2015) devel- among minority youth and cultural factors that
oped a web-delivered CBT intervention, called may reduce acceptability and efficacy of existing
Bounce Back Now. In an RCT of 987 tornado- interventions, examining cultural adaptations to
impacted adolescents, the researchers found evidence-based treatments for pediatric PTSD is
fewer PTSD symptoms at postintervention com- an important avenue of research. A recent review
pared to no-intervention control group. The summarized such adaptations for trauma-specific
researchers highlighted the benefit of population- CBTs (Ennis et al., 2020). Seventeen studies
based recruitment and increasing access to care. were identified and adaptations ranged from
translations only to inclusion of additional com-
ponents (e.g., family sessions). Fourteen studies
Multiply Traumatized Youth evaluated the adapted treatments and found
favorable outcomes, with only a few evaluating
Studies have shown that youth who experience efficacy through RCTs, precluding firm conclu-
multiple traumas present with more complex sions. More research is needed to determine the
symptomatology (e.g., Ross et al., 2021). potential need for cultural adaptations and to
TF-CBT can be tailored to the domains that are evaluate the relative efficacy of established treat-
problematic with complex trauma (Cohen et al., ment protocols compared to adapted ones.
2012). In a study of 176 youth-parent dyads,
TF-CBT was found to be effective in decreasing
complex PTSD symptoms in youth who experi- Treatment Modality
enced chronic and acute trauma (Ross et al.,
2021). A study of 842 youth (ages birth-18 years Trauma-specific CBT is typically delivered indi-
old) in the welfare system with complex trauma vidually with conjoint parent training and family
compared the effectiveness of TF-CBT, sessions for sharing the trauma narrative. TF-CBT
Attachment, Self-regulation, and Competency has been adapted to be delivered in groups
(ARC), and Child-Parent Psychotherapy (Bartlett (Deblinger et al., 2016). Mavranezouli et al.’s
et al., 2018). All models resulted in improve- (2020) meta-analysis of treatments for pediatric
ments in PTSD symptoms, with the best out- PTSD found that the group version of TF-CBT
comes for TF-CBT and ARC. demonstrated a large effect size. CBITS, described
earlier, is delivered in a group format in schools
and has been shown to be efficacious for reducing
Cultural Considerations PTSD symptoms in diverse populations.
Group interventions confer important unique
Researchers examining cultural factors in the benefits relative to individual treatments, includ-
treatment of pediatric PTSD have focused pri- ing increased availability and cost-effectiveness
marily on race and ethnicity. Children and adults of services, opportunities for training (e.g., live
of color and from lower socioeconomic back- supervision of less experienced clinicians), and
grounds are more likely to be exposed to trauma increased social support among both children and
(e.g., Curran et al., 2018) and, in turn, have higher caregivers (Deblinger et al., 2016). Group inter-
levels of PTSD (e.g., Andrews et al., 2015). ventions also are well-suited for community-
Community-based trials that include multicul- level traumas such as community violence and
tural youth have demonstrated the effectiveness natural disasters due to their reach and relative
of TF-CBT, both with and without adaptations efficiency of implementation. It is important to
(e.g., Ross et al., 2021; Stewart, Orengo-Aguayo, note that both TF-CBT group and CBITS require
individual sessions for the imaginal exposure
component. More investigations are needed that sizes of treatment outcome studies. Nonetheless,
directly compare evidence-based group treat- evidence suggests that several additional factors
ments to established individual treatments dis- may impact treatment outcome. Trauma-specific
seminated in the same setting. CBTs appear to be more efficacious among older
youth compared to younger children (Dorsey
et al., 2017; Gutermann et al., 2016; Miller-Graff
Caregiver Participation in Treatment & Campion, 2016). Some have found that treat-
ment effects are smaller among those with more
Evidence supports the participation of the nonof- severe PTSD at baseline (Miller-Graff &
fending parent or caregiver in the treatment of Campion, 2016), although studies also suggest
traumatized youth. Caregiver involvement may that existing trauma-specific CBTs may be just as
not be necessary, however, for youth PTSD efficacious for complex PTSD presentations
symptom reduction. In an early meta-analysis, (Ross et al., 2021). Emerging research suggests
Silverman et al. (2008) found that the inclusion that improvements in maladaptive cognitions
of parents was associated with more effective during TF-CBT are predictive of degree of PTSD
treatment of only child anxiety and depression, reduction (Pfeiffer et al., 2017). Additional fac-
but not PTSD symptoms. Two recent meta- tors, including family-level variables (cohesion/
analyses similarly found that treatments for pedi- conflict, caregiver psychopathology) and treat-
atric PTSD with and without caregiver ment format (with or without caregiver involve-
participation yielded similar effect sizes ment), warrant further examination.
(Gutermann et al., 2017; Miller-Graff &
Campion, 2016). A recent review of caregiver
involvement in TF-CBT (Brown, Cohen, & Limitations of Current Research
Mannarino, 2020) summarized the literature on on the Treatment of Pediatric PTSD
the effects of TF-CBT on caregiver symptoms
and the potential role of changes in caregiver fac- The efficacy research for the treatment of pediat-
tors in children’s symptom improvement. The ric PTSD is robust. That said, given the preva-
authors concluded that during TF-CBT, caregiv- lence of trauma exposure and subsequent mental
ers improve in their own depressive symptoms health problems, we recommend more effective-
and distress (Martin et al., 2019), and that care- ness research, particularly dissemination and
givers’ processing of their own cognitive and implementation science. We need research exam-
emotional responses to trauma predict changes in ining treatments for complex or multiple types of
child internalizing and externalizing, but not traumas (i.e., poly-victimization), particularly
PTSD symptoms (Yasinski et al., 2016, 2018). across ecological contexts (e.g., family and com-
Dorsey et al. (2017) highlighted that caregiver munity violence), and those with significant
involvement continues to be empirically sup- comorbid psychopathology (e.g., substance use;
ported in the treatment of pediatric PTSD, noting Hahn et al., 2020). Additionally, research is lim-
that specific characteristics (e.g., very young ited on the efficacy of trauma-specific CBTs in
children, parents’ trauma-related distress) may higher levels of care (e.g., inpatient, residential),
warrant caregiver involvement. despite high prevalence of trauma histories for
youth in these settings. Given that trauma-specific
CBTs are more efficacious for older (versus
Additional Factors Related younger) children (Miller-Graff & Campion,
to Treatment Outcome 2016), empirical evaluation of developmental
adaptations to existing treatments (e.g., Pollio &
Few studies have been able to examine mediators Deblinger, 2017) may increase effectiveness for
and moderators of evidence-based treatment of this vulnerable population, who are likely to
PTSD in youth due to relatively small sample require significant caregiver involvement.
Relatedly, the study of caregivers in the treatment treatments are most/least efficacious. This work
of pediatric PTSD may be particularly salient for will in turn inform much-needed work on increas-
traumas that occur within the family context (i.e., ing the accessibility and availability of evidence-
maltreatment). Further work is needed to empiri- based services for youth who most need them,
cally identify the subset of children for whom the including using alternative delivery methods
involvement of a supportive adult may be critical (e.g., telehealth), to increase their reach.
for the reduction of PTSD symptoms.
Additionally, research focusing on correlates of
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Treatment processes and demographic variables as
Obsessive-Compulsive Disorder
Allie N. Townsend, Johann M. D’Souza,
Andrew G. Guzick, and Eric A. Storch
Background form in an attempt to alleviate distress or prevent

feared outcomes. Although the presence of either
Obsessive-compulsive disorder (OCD) is a psy- obsessions or compulsions is sufficient to meet
chiatric disorder that impacts 1–2% of children diagnostic criteria, the two almost always occur
and adolescents (Canals et al., 2012; Barzilay together (Foa et al., 1990).
et al., 2019) and is characterized by the presence Clinical presentations of OCD vary substan-
of obsessions and compulsions to the extent that tially but tend to cluster around four main catego-
there is significant distress or impairment in time ries or dimensions of obsessional content. These
and/or functioning (American Psychiatric include contamination, harm, taboo/unacceptable
Association [APA], 2013). Obsessions are thoughts, and symmetry, although harm and
defined as intrusive and recurrent thoughts or taboo are sometimes included in the same dimen-
images that are distressing and unwanted. sion (Abramowitz et al., 2010; Bloch et al.,
Compulsions are repetitive behaviors or mental 2008). Most youth experience symptoms across
acts that the individual feels compelled to per- multiple dimensions (Rosario-Campos et al.,
2006). Childhood OCD tends to continue into
adulthood, and 30–50% of adults with OCD
report onset of symptoms in childhood (March
et al., 2001).
A. N. Townsend
Department of Psychiatry and Behavioral Sciences,
The Chicago School of Professional Psychology, Developmental Features
Washington, DC, USA and Considerations
J. M. D’Souza
Department of Psychiatry and Behavioral Sciences, Biological Factors
Department of Psychology, University of Houston, Although the exact etiology of OCD is unknown,
Houston, TX, USA it likely results from a combination of various
Texas Institute for Measurement, Evaluation, and genetic, neurobiological, and psychological fac-
Statistics, University of Houston, Houston, TX, USA tors. Genetic models have demonstrated that the
A. G. Guzick · E. A. Storch (*) heritability of child onset OCD is 0.43, which
Department of Psychiatry and Behavioral Sciences, yields higher genetic loading compared to adult-
Baylor College of Medicine, Houston, TX, USA onset OCD (Arnold et al., 2018). Twin studies
e-mail: Eric.Storch@bcm.edu
https://doi.org/10.1007/978-3-031-14080-8_22
332 A. N. Townsend et al.
have demonstrated that up to 50% of OCD symp- riencing excessive distress when not completing
tom variability is heritable, with no gender differ- the ritual are signs of OCD symptoms. Therefore,
ences noted (Mataix-Cols et al., 2013). On the normative rituals are distinguished from OCD in
other hand, shared environmental factors do not their levels of associated distress, duration, and
impact the etiology of OCD (Mataix-Cols et al., functional impairment.
2013). No specific genes have been identified in
OCD, although the glutaminergic system appears
to be implicated (Arnold et al., 2018). Early-Onset OCD
Neurobiological data on individuals with
OCD implicate the cortico-striato-thalamo- Age of onset has been identified as an important
cortico (CSTC) circuits of the brain (Pauls et al., factor in differentiating various OCD presenta-
2014). In addition, individuals with OCD tions. Early-onset OCD, which typically refers to
uniquely demonstrate impairments in the direct symptoms arising during childhood or early ado-
and indirect pathways between the orbitofrontal lescence, tends to have some differing features
cortex and subcortical regions (Pauls et al., 2014). from adult-onset OCD (Taylor, 2011). Early-
It is postulated that excessive activity in the direct onset OCD is associated with a stronger genetic
pathway, which is usually inhibited by the indi- contribution than adult-onset OCD (Arnold et al.,
rect pathway, directly contributes to repetitive 2018). Regarding gender, males tend to have
thinking and behaviors seen in OCD. Further early-onset OCD more commonly than females;
neurobiological factors that have been found to however, this gender discrepancy appears rela-
be implicated in OCD include differences in glu- tively even by adolescence (Mathes et al., 2019).
tamatergic and serotonergic systems and Further, nearly 25% of males with OCD have
increased amygdala sensitivity (Pauls et al., onset before age 10, while the highest frequency
2014). Psychological factors contributing to of onset in females is during adolescent years
OCD are discussed in the treatment section (Ruscio et al., 2010). Compared with adult-onset
below. OCD, those with an earlier onset also tend to
have higher tic disorders comorbidity (Geller
et al., 2001; Taylor, 2011); internalizing and
Normative Versus Pathological externalizing psychopathology are associated
with OCD across the lifespan (Lebowitz et al.,
In the treatment of child and adolescent OCD, it 2011). Further, early-onset OCD is linked to
is important to differentiate normative fears and future psychiatric diagnoses during adulthood,
repetitive behaviors from pathological obsessive- including obsessive-compulsive personality dis-
compulsive symptomatology. Insistence on order, eating disorders, and panic disorder (Pinto
sameness, motor stereotypies, and ritualized et al., 2006).
behaviors are a normal part of development in
children (Evans et al., 2017). These behaviors are
biologically adaptive and foster emotional regu- Insight
lation. Such rituals can be seen during routines
around transition periods (bedtime, bath time, Most adults and adolescents tend to have good
mealtime), during play and game time, and in insight into the irrational and peculiar nature of
response to normative developmental fears (dark- their symptoms; however, this can be more vari-
ness, monsters; Bolton et al., 2009). However, able in youth. The association between age and
similar ritualized behaviors can be indicative of insight has been found to increase across the
OCD when they are experienced as distressing, lifespan such that younger children tend to have
take significant amounts of time, and interfere less insight into symptoms compared to adoles-
with activity initiation and completion. Further, cents, and youth in general, less than adult popu-
completing the ritual excessively as well as expe- lations (Geller, 2006; Selles et al., 2014). Further,
22 Obsessive-Compulsive Disorder in Children and Adolescents 333
poor insight in youth is associated with ADHD OCD impairs the affected child’s home func-
prevalence and younger age, which may reflect tioning as well as all others living in the home by
relative cognitive development; as youth with disrupting daily routines for the entire family,
OCD continue to develop metacognition (the especially morning, nighttime, and mealtime rou-
ability to “think about thinking”), they may expe- tines (Stewart et al., 2017). Intrusive thoughts
rience increased insight as well (Selles et al., and just-right compulsions were found to most
2018). Low insight in childhood OCD has been significantly hinder family functioning. Poor
associated with increased disorder-related insight is associated with greater disruptions in
impairment and family accommodation (Storch social and home functioning (Storch et al., 2010).
et al., 2008). Insight in OCD has been found to be Specifically for parents, 45% of mothers and one-
associated with symptoms severity and treatment third of fathers endorse occupational impairment
outcomes across time such that poorer insight related to their child’s symptomatology (Stewart
often yields more severe presentations, increased et al., 2017).
risk for comorbidities, and less successful treat- Emotionally, parents and children with OCD
ment (Selles et al., 2018; Storch et al., 2008; report stress and/or anxiety as the most impactful
Visser et al., 2017). Specifically, poor insight in on their functioning (Stewart et al., 2017). Parents
youth is associated with decreased symptom of children with OCD are uniquely associated
resistance as well as increased distress and avoid- with increased rates of psychopathology. For
ance behaviors (Selles et al., 2018). example, mothers of children with OCD show
higher rates of depression and anxiety than moth-
ers of children with anxious and non-clinical pre-
Impact sentations (Barrett et al., 2002; Murphy &
Flessner, 2015; Smorti, 2012). This likely reflects
OCD has been shown to have adverse effects on a bidirectional relationship, as there is a height-
a child’s academic, social, and familial function- ened genetic risk for depression and anxiety in
ing (Wu et al., 2018). Nearly 90% of children parents of youth with OCD, though raising a
with OCD experience impairment in one of these child with OCD can be stressful in it of itself.
domains, and about half experience impairment Parent and child reports of impairment often
in all three domains (Piacentini et al., 2003). differ, thus showing the need to evaluate both the
Severity of impairment is associated with symp- parent’s and child’s perceived functional impair-
tom severity, comorbid diagnoses, level of ment (Piacentini et al., 2003). Overall, parents
insight, and family accommodation (Geller et al., are more likely to report more severe impairment
2003; Nadeau et al., 2013; Storch et al., 2007b). than children, especially when it comes to aca-
Obsessive symptoms have been found to be more demic and family functioning. However, there
strongly linked to functional impairment than are few areas that children tend to report higher
compulsive or avoidant behaviors (De Caluwé severity than their parents, specifically leisure
et al., 2014; De Caluwé & De Clercq, 2015). activities that require concentration and academic
In regard to academic functioning, both the or social situations wherein their parent is not
affected child and their parent report impairments present (Piacentini et al., 2003; Stewart et al.,
in the child’s ability to concentrate on school- 2017). Overall, children are less likely to report
work and complete homework assignments impairment, except with regard to school func-
(Piacentini et al., 2003). In fact, a population- tioning perhaps because children are less likely to
based study in Sweden found that individuals notice impairment in settings where parental
with OCD diagnosed before age 18 demonstrate accommodation is possible (Storch et al., 2010).
reduced educational attainments across all educa- At school, children have mandatory activities that
tion levels from compulsory schooling through are completed without family members who
postgraduate education (Pérez-Vigil et al., 2018). accommodate, which yields increased awareness
of their functional impairments.
Family Factors washing behaviors together with a child, or other

excessive washing (e.g., doing extra laundry).
Family Accommodation Further, fears of germs are easier to endorse than
Many children with OCD seek parental support more stigmatized OCD fears (e.g., harming self
which unwittingly results in exacerbation of or others), which may increase the likelihood a
symptomology. This caregiver participation, child would voice these fears to their parents and
often termed family accommodation, can include insist on their participation in compulsions or
direct engagement with compulsive behaviors, avoidance. Comorbid child psychopathology,
allowance and promotion of avoidant behaviors, specifically externalizing behaviors, ADHD, and
alterations of familial functioning, and ODD, have been associated with increased famil-
reassurance-giving that all serve to maintain and/ ial accommodation (Wu et al., 2019).
or exacerbate the child’s OCD symptoms (Benito
et al., 2015; Flessner et al., 2011; Wu et al., 2018, arent-Child Conflict and Hostility
P
2019). Family accommodation is particularly Given the high level of family involvement in
salient for children with OCD, as up to 97% of child and adolescent OCD, it is unsurprising that
families endorse engaging in family accommoda- there would be increased rates of relational con-
tion and about half of the families do so on a flict and distress within the family. Although
daily basis (Peris et al., 2008; Wu et al., 2019). family accommodation is virtually ubiquitous,
These behaviors are most often done to alleviate significant familial conflict is only a problem for
the child’s distress, minimize activity interrup- a subset of families. Multiple factors impact
tion, or avoid unwanted behavioral outbursts (Wu parent-child conflict, including family accommo-
et al., 2019). Despite short-term mitigations of dation, parental characteristics, and communica-
distress, the family accommodation is negative tion style.
over the long term as it prevents the child’s expo- Family accommodation, as previously men-
sure to feared situations, the associated corrective tioned, has negative impacts on both the child
learning that occurs, and negatively reinforces and family members. Higher family accommoda-
avoidance behavior through short-term reduction is associated with elevated family conflict
tions in distress that follow accommodation (Peris et al., 2008). From a purely practical stand-
(Benito et al., 2015; Storch et al., 2007a, b; Wu point, involving family members in avoidance
et al., 2019). and ritual behaviors is inconvenient and can take
Family accommodation has been positively a significant amount of time depending on fre-
associated with child OCD severity and func- quency and duration. With caregivers specifi-
tional impairment, insinuating a bidirectional cally, parents report personal distress related to
impact of more severe OCD and increased the provision of accommodation. Further, parents
accommodation (Thompson-Hollands et al., often report that the affected child will show
2015; Wu et al., 2016, 2019). Familial accommo- anger and/or behavioral outbursts in response to
dation presents across OCD presentations; how- parent refusal of accommodation (Storch et al.,
ever, it has been found to be highest in 2012; Wu et al., 2019). These anger outbursts are
contamination subtypes and lowest in harm/sex- especially relevant for children with comorbid
ual subtypes (Wu et al., 2019). The increased disinhibition difficulties, emotional dysregula-
accommodation in contamination subtype could tion, and oppositional behavior (Lebowitz et al.,
be the result of increased opportunity for accom- 2011; Wu et al., 2019). Therefore, their decision
modation throughout the day, such as during to resist or provide accommodation can result in
mealtime, bedtime routines, and other household increased parental distress, guilt, and feelings of
activities, or may also be related to the overt, blame toward the affected child (Murphy &
explicit nature of contamination compulsions Flessner, 2015; Peris et al., 2008).
that parents are likely to get involved with, such In regard to parent characteristics, psychopa-
as preparing food a specific way, engaging in thology and levels or organization/cohesion are
indicated in parent-child conflict. Parent psycho- Clinician-Administered Measures

pathology is implicated such that parents with
higher hostility and psychopathology broadly CD Symptoms and Severity
O
assessed are more likely to accommodate their The Children’s Yale Brown Obsessive Compulsive
child’s OCD (Peris et al., 2008). Furthermore, Scale (CY-BOCS) is a clinician-administered,
parents with elevated hostility and psychopathol- semi-structured interview to assess OCD symp-
ogy are more likely to perceive the consequences toms and severity (Scahill et al., 1997). It is the
of resisting accommodation as detrimental. This most commonly utilized assessment for OCD
is relevant in that perceived negative outcomes of and has two main components. The initial com-
resisting accommodation can increase the likeli- ponent of the CY-BOCS is a 61-item checklist
hood of parental accommodation. Organized and that identifies current (within the past week) and
cohesive families demonstrate fewer routine past (ever during the lifetime) obsessions and
accommodating behaviors and distress related to compulsions. The next portion is a measurement
accommodation (Peris et al., 2008; Wu et al., of symptom severity, with ten items scored 0–4
2014). Likert scale, with items assessing time, impair-
Communication styles of parents and the ment, interference, and distress associated with
affected child are indicated in parent-child hostil-
symptoms as well as the individual’s resistance to
ity. Parental communication that is characterized and control over the symptoms. The CY-BOCS
as critical and harsh is associated with more has well-established psychometric properties,
severe OCD presentations (Przeworski et al., including high internal consistency, convergent
2011; Peris et al., 2008). Maternal criticism has and divergent validity, test-retest reliability, and
been found to be more elevated in communica- interrater reliability (Scahill et al., 1997; Storch
tion with their child with OCD compared to an et al., 2004).
unaffected sibling (Przeworski et al., 2011). The second edition of the measure
Furthermore, increased familial communication (CY-BOCS-II) was created in order to provide
dysfunction and parental hostility are associated necessary updates given the increased research
with diminished treatment response (Peris et al., and understanding of the disorder in recent years
2012). (Storch et al., 2019). The four major updates of
the measure were: adding in measurement of
avoidance symptoms; expanding the severity
Assessment Likert scale from 0 to 4 to 0 to 5 to allow for
increased sensitivity for severe presentations;
Clinician-administered assessments are consid- replacing the “resistance of obsessions” item
ered gold standard; however, child and parent- with a “obsession-free interval” item, as gold
report measures are useful when limitations in standard therapy encourages acceptance/toler-
time, training, or resources are present. OCD ance of obsessions rather than “resistance,” and
measures that comprehensively assess the breadth consequently, psychometric properties for this
and severity of symptoms as well as more pointed item were mixed; and updating/re-organizing the
measures for associated sequalae such as family symptom checklist to minimize confusion and
accommodation, cognitive beliefs, and functional increase utility. Initial assessment of the mea-
impairment have been created and validated. The sure’s psychometric properties exhibits moderate-
following provides a non-inclusive list of well- to-strong internal consistency, excellent interrater
established measures that are useful in assessing reliability, and test-retest reliability (Storch et al.,
childhood OCD. 2019).
Family Accommodation
The Family Accommodation Scale for Obsessive
Compulsive Disorder-Interviewer Rated
(FAS-IR) is a clinician-administered, semi- Cognitive Beliefs

structured interview to assess parental accommo- The Obsessive Belief Questionnaire-Child
dation behaviors (Calvocoressi et al., 1999). The Version (OBQ-CV) is a 44-item questionnaire
assessment measures the presence of 12 accom- that assesses beliefs and cognitions related to
modating behaviors within the past week, as well childhood OCD (Coles et al., 2010). Beliefs
as the frequency of each behavior being rated on assessed include heightened sense of responsibil-
a 0 (no/not applicable) to 4 (every day/extreme) ity, perceptions of threat, perceived importance
Likert scale. The measure has demonstrated high of one’s thoughts and the need to control them,
internal consistency, convergent and divergent and need for certainty. The OBQ-CV has demon-
validity, and interrater reliability (Calvocoressi strated internal consistency, test-retest reliability,
et al., 1999). and convergent validity.
OCD-Related Impairment
Parent and Self-report Measures Based on the Child Obsessive-Compulsive
Impact Scale (Piacentini & Jaffer, 1999), the
Although clinician-administered measures are Child Obsessive-Compulsive Impact Scale-
considered to be most ideal in accurately assess- Revised (COIS-R) is a measure specifically
ing OCD symptoms and severity, there are parent designed to measure OCD-specific impairment
and self-report measures that can be used when (Piacentini et al., 2007b). The COIS-R is a
comprehensive, clinician-scored measures are 33-item questionnaire that has child-report and
not feasible. parent-report versions. The parent-report version
has a four-factor structure consisting of impair-
CD Symptoms and Severity
O ment in daily living skills, school, social, and
The Children’s Florida Obsessive-Compulsive family/activities, whereas the child-report ver-
Inventory (C-FOCI) is a brief screening measure sion has a three-factor structure consisting of
that assesses OCD symptoms and severity (Storch school, social, and activity impairments. Both
et al., 2009). The symptom component includes a measures have good internal consistency, concur-
17-item checklist of common obsessions rated as rent validity, and test-retest reliability (Piacentini
not present or present. The second component is et al., 2007a, b).
a unitary severity scale that assesses time, dis- The OCD Family Functioning Scale (OFF)
tress, avoidance, interference, and control of was created to assess the context, extent, and per-
symptoms. The C-FOCI demonstrates good spectives of functional impairment for family
internal consistency, convergent and divergent members of an individual with OCD (Stewart
validity, and treatment sensitivity (Storch et al., et al., 2011). OFF is a 42-item measure that
2009). assesses impairment in three components: family
The Obsessive-Compulsive Inventory-Child functioning, symptom-specific, family role-
Version (OCI-CV) is another brief self-report specific domains. There are versions for both the
measure for child and adolescent OCD (Foa family members and the affected individual; both
et al., 2010). This measure assesses 21 common versions demonstrate excellent internal consis-
obsessions and compulsions across the six symp- tency, good convergent validity, and test-retest
tom domains of washing, hoarding, ordering, reliability.
checking, harm-related obsessions, and neutral-
izing. The psychometric properties of the Family Accommodation
OCI-CV are strong, including good test-retest The Family Accommodation Scale for OCD-
reliability, internal consistency, and convergent Self-Rated Version (FAS-SR) was created to pro-
validity (Foa et al., 2010; Jones et al., 2013). mote further collection of family accommodation
data when the FAS-IR is not feasible (Pinto et al.,
2013). The FAS-SR is a family-member-report
measure that, similar to the FAS-IR, evaluates thewhen a previously neutral stimulus (e.g., bath-
presence and frequency of accommodating room) is paired with an unconditioned stimulus
behaviors. The measure demonstrates excellent (e.g., germs) that evokes a response (anxiety).
internal consistency, convergent validity, and Once classical conditioning establishes an asso-
strong agreement with the FAS-IR. ciation between the previously neutral stimulus
The Family Accommodation Scale Anxiety and the fear response, the fear develops and is
(FASA) was developed as a modified version of then maintained via operant conditioning.
the FAS that broaden the assessment scope to Specifically, operant conditioning in anxiety pro-
include children with anxiety disorders beyond poses that avoidance and compulsions provide
OCD (Lebowitz et al., 2013). The FASA is a temporary relief from distress, and thus these
parent-report measure that evaluates family strategies are more likely to occur again in simi-
accommodation and associated parental distress. lar situations. The relief that follows the avoid-
The FASA-child report (FASA-CR) is the child ance and compulsive behaviors prevents new
version of the FASA that assesses the frequency learning to occur and negatively reinforces avoid-
and associated schedule/routine modification ance/compulsions, as these behaviors are more
(Lebowitz et al., 2015). Additional, non-weighted likely to be performed again due to the short-term
questions assess associated parental distress, decrease in distress that follows.
child reactions, and child beliefs about the In regard to cognitive conceptualization, mal-
accommodation. Psychometric properties for the adaptive interpretations of intrusive thoughts are
FASA and FASA-CR are sound (Lebowitz et al., believed to contribute to symptom development.
2015, 2016). Most individuals experience intrusive thoughts;
The Pediatric Accommodation Scale (PAS) however, individuals with OCD interpret these
measures family accommodation for youth with thoughts differently. Specific cognitive misap-
anxiety disorders (Benito et al., 2015). The PAS praisals indicated in OCD development and
has two versions, a clinician-rated (PAS) and a maintenance are perceived sense of responsibil-
parent-rated (PAS-PR) version. The measures ity and over-evaluation of the importance of
were developed simultaneously, and both assess intrusive thoughts (Coles et al., 2010).
the frequency and impact of family accommoda- Furthermore, a subset of individuals with OCD
tion. The PAS demonstrated strong psychometric will experience thought-action fusion, or the
properties, including internal consistency, inter-
belief that having thoughts about a certain event
rater reliability, and convergent and discriminantincreases the likelihood that the event will occur
validity. The PAS-PR demonstrated good internal or is morally equivalent to the event occurring
consistency and convergent validity with the (Evans et al., 2011). This phenomenon is related
PAS. to insight, which as previously mentioned, is
associated with poorer treatment outcomes.
Taken together, children and adolescents with
Treatment OCD experience intrusive thoughts, associated
distress, and then engage in compulsive behav-
Conceptualization iors in order to alleviate their distress. The
repeated engagement with compulsive behaviors
The strongest empirical support for psychologi- and avoidance strategies establishes the OCD
cal models of OCD is those within cognitive- cycle and maintains the disorder. Notably, par-
behavioral theory (CBT). Mowrer’s two-factor ents and family members often become involved
theory, which serves as the primary behavioral in this cycle through accommodation behaviors,
model, postulates that classical conditioning and as a result, serve to maintain and/or exacer-
establishes the fear and operant conditioning bate the disorder. Therefore, treatment includes
maintains the fear via negative reinforcement both child and, to varying extents, parent/family
(Mowrer, 1960). Classical conditioning occurs involvement.
Cognitive-Behavioral Therapy that parents understand that accommodating mal-

with Exposure and Response adaptive thoughts and behavior maintains symp-
Prevention toms in the long-term despite temporary anxiety
relief in the short term.
The most effective treatment approach for OCD
in children and adolescents is CBT, and more Hierarchy Development
specifically, exposure and response prevention To introduce the fear hierarchy, the therapist can
(ERP; Piacentini et al., 2007a). The general goal explain that, like acquiring any skill, fighting
of ERP is to expose the individual to triggers that OCD will take regular practice over time. The
provoke obsessions while reducing, and eventu- hierarchy or “fear ladder” provides the treatment
ally eliminating the use of compulsive rituals or plan with progressively more distressing chal-
safety behaviors. ERP allows the person to learn lenges building from 0 to 10. Children may ben-
that their fears are not dangerous and that they efit from visual aids such as a step ladder, and
can tolerate and manage them (Freeman et al., very young children may benefit from a non-
2018). ERP is a stepwise treatment that consists numerical scale such as green-yellow-red or
of psychoeducation, functional assessment, hier- easy-medium-hard. The hierarchy should aim to
archy development, ERP, and relapse prevention. identify symptomatology that will be addressed
Additional components are often utilized in the in treatment including avoided situations and
treatment of children to target the familial thoughts, rituals, and family accommodating
involvement and engage the child in a develop- behaviors.
mentally appropriate fashion.
xposure and Response Prevention
E
Psychoeducation Once the hierarchy is created, the therapist
The program begins with psychoeducation on the engages the child in exposures to the feared stim-
nature of the disorder and the rationale for the uli. Exposures typically proceed from least dis-
treatment. Given that there is some reluctance tressing to most in order to build confidence and
among therapists and patients to engage in expo- buy-in, however, proceeding in a modestly non-
sure therapy due to a fear of perceived negative linear fashion may help generalize the effective-
consequences, psychoeducation is important in ness of exposure (Craske et al., 2014). Exposures
clarifying that exposure therapy is both very safe can be imaginal (e.g., saying “God is mad at me
and very effective (Schneider et al., 2020). ERP right now”) or in vivo (e.g., touching the floor
manuals for children describe ERP as “bravery without washing hands). During and after these
practice” or an opportunity to “boss back” OCD exposures, the child strives to prevent compul-
(March & Benton, 2006; Storch et al., 2018). sions or rituals to allow new learning to occur. If
Obsessions can be described as “brain hiccups” the child gives into a compulsion, the therapist
with the resulting anxiety described as “false works with a family to try the exposure again, or
alarms.” OCD is externalized as the enemy to alternatively, temporarily reduces the exposure
fight (e.g., “I understand that OCD is making you goal so the child is able to complete it success-
do things you don’t want to do”; “what is OCD fully (for example, by taking only one step in an
telling you to do?”). This serves as (1) a type of arranging compulsion rather than eliminating it
cognitive defusion strategy and (2) a way for the completely). A historical rule of thumb is that the
parent and child to team up against the OCD and exposure is endured until the child’s subjective
minimize conflict with each other. In addition to distress habituates to half the amount at the peak
psychoeducation for the child, psychoeducation of the exposure, though recent research has dem-
for the family is important as it serves to reduce onstrated that this habituation is not necessary to
child blaming for irrational beliefs and behaviors promote treatment outcomes (Craske et al.,
as well as identify ways to reduce accommoda- 2014). This guideline may still hold value as it
tion of these beliefs and behaviors. It is essential ensures that exposures are conducted for a suffi-
cient period of time, and when fear reduces with- incentive. Children can be motivated by simple
out using compulsions, it may be indicative of an rewards such as stickers while adolescents can
extinction learning processes (Benito et al., exercise increasing independence by picking
2018). their own rewards. Regardless of age, sometimes
Violating feared expectations is considered to the best reward is genuine praise for sincere
be an important marker of extinction learning effort, which simultaneously encourages a
during exposure. Cognitive techniques can be growth mindset. As a further aid, family mem-
used to consolidate learning by asking the child bers are taught to disengage in their child’s rituals
what they fear will happen before the exposure over time as a way of increasing the child’s self-
and then asking them after the exposure if their efficacy and thereby fostering long-term gains.
feared consequence occurred. Feared expecta- Finally, it is important to note that parents and
tions may range from specific feared outcomes family members may struggle observing their
(e.g., “my Mom will die if I don’t repeat the num- child in distress during exposures, and the subse-
ber 3”) to simply expecting that the exposure will quent relationship conflict that OCD can bring.
provoke too much distress (e.g., believing they Therefore, the therapist can also help family
can’t endure the “not right” feeling if socks are members cope with their own distress (Peris
not pulled to the same length). In many cases, the et al., 2008).
feared outcome will not be immediately refutable ERP has been manualized for children as
(e.g., going to Hell for saying a bad word, getting young as 5–8 years old (Freeman & Garcia,
brain cancer from standing next to a working 2008), with demonstrated efficacy (Freeman &
microwave). In those cases, it may be more Garcia, 2008; Freeman et al., 2014; Lewin et al.,
important to emphasize tolerance of distress and 2014). Adaptations for this age group include
uncertainty (“Look at that, you did it even though treating parents as coaches who help their chil-
it was super scary! You’re so brave!”). In other dren successfully implement ERP. Parents
cases, the feared outcome may actually occur accomplish this by learning behavior modifica-
(e.g., a child with obsessions about being bitten tion strategies for their children while also grow-
by insects may get bit by an ant during exposure ing in awareness of their own anxiety.
bite). Those may also be cases when tolerating Additionally, parents learn to communicate with
distress better than anticipated would be a helpful their children about thoughts and emotions while
strategy. In fact, there is some reason to believe learning ways to increase their child’s treatment
exposures that occasionally result in the feared adherence and motivation.
outcome could enhance treatment outcomes
through promoting distress tolerance and prepar- Relapse Prevention
ing youth adequately for future challenges when To prevent relapse, parent and therapist should
negative events do occur (Krompinger et al., emphasize their confidence in the child’s ability
2019). to continually implement the strategies to fight
To increase engagement, the therapist can OCD. To consolidate learning, the therapist can
help the child turn exposures into a game such as ask the child to identify the most helpful strate-
the therapist and child or parent and child daring gies used in treatment. In addition, the therapist
each other to touch more and more contaminated can help the child anticipate and address future
objects. Using rewards or a token economy to challenges. Finally, the child is encouraged to
reinforce participation in ERP can also be a help- monitor the battle with OCD and let their parent
ful engagement strategy during therapy. know if they need extra help with a therapist
again. Creating a book or personalized treatment
Parent Involvement guide identifying the most effective strategies,
Parents are very important in facilitating between- predicted challenges, and warning signs of
session exposures, in other words, adherence to required treatment re-initiation can be a fun,
homework. Rewards can be used as a behavioral effective way to consolidate essential informa-
tion for the child to reference following treatment delivered CBT, especially if access to face-to-
termination. face services is difficult.
Delivery Options for CBT Pharmacotherapy
Typically, ERP is delivered in a weekly, face-to- In addition to ERP, certain medications have been
face therapy session. Modified versions of OCD shown to be effective in the treatment of child
treatment include brief CBT, intensive CBT, and adolescent OCD. Serotonin reuptake inhibi-
Internet-based CBT, and parent only approaches. tors (SRIs) are the pharmacological treatments
There is some research on the effectiveness of with the strongest empirical base (Geller &
brief CBT consisting of a reduced number of ses- March, 2012). The United States Food and Drug
sions. For example, one study of OCD in children Administration (FDA) has approved clomip-
and adolescents found that both brief CBT and ramine (Anafranil) for ages 10 and older, fluox-
full CBT led to statistically significant symptom etine (Prozac) for ages 7 and older, fluvoxamine
improvement as compared to waitlist control, (Luvox) for ages 8 and older, and sertraline
whereas there was no statistically significant dif- (Zoloft) for ages 6 and older to treat OCD in chil-
ference in the effectiveness of brief CBT versus dren and adolescents (Hieber, 2013).
full CBT in symptom improvement (Bolton et al.,
2011). This is likely not a clinically viable
approach for those with moderate and higher Treatment Efficacy
symptomology. On the other extreme, intensive
treatment can include daily rather than weekly Several reviews and meta-analyses report the
sessions for convenience (taking advantage of effectiveness of these psychological and pharma-
holidays), quicker outcomes, or severity of symp- cological treatment approaches. CBT for child
toms (Storch et al., 2007a, b; Riise et al., 2018). and adolescent OCD has robust empirical sup-
In complex cases of childhood OCD, parents port compared to various psychological and med-
may benefit from an intervention focused on ication comparison conditions (McGuire et al.,
managing their own stress. The manual Helping 2015; Öst et al., 2016). Regarding medications,
Parents Manage Childhood OCD: Decreasing the first-generation antidepressant clomipramine
Conflict and Increasing Positive Interaction showed a statistically significantly higher effect
describes a brief intervention meant to comple- size as compared to SRIs, though this medication
ment exposure and response prevention (Peris & is less frequently prescribed now as it is only
Piacentini, 2016). marginally more effective and has a more adverse
ERP can also be implemented using technol- side-effect profile (Decloedt & Stein, 2010).
ogy. Telehealth-delivered CBT has demonstrated Among studies assessing both CBT and medi-
efficacy relative to waitlist (Storch et al., 2011). cation treatment efficacies, one meta-analysis
Internet-delivered CBT for adolescents shows a found that CBT was superior to comparison con-
strong effect in reducing OCD symptoms as com- ditions with a very large effect size (10 studies;
pared to a waitlist control (Lenhard et al., 2017; g = 1.21) while SRIs were superior to control
Storch et al., 2011). A more recent study found conditions with a moderate effect size (11 stud-
that Internet-delivered CBT had fewer respond- ies; g = 0.50; McGuire et al., 2015). Another
ers than face-to-face CBT, although this outcome meta-analysis found that CBT had a very large
was attenuated when non-responders from both effect on symptom improvement compared to
groups received additional face-to-face CBT ses- waitlist or placebo, and SRI medication had a
sions (Aspvall et al., 2021). This study suggests moderate effect size compared to placebo (Öst
that many adolescents can benefit from Internet- et al., 2016). This study further found that CBT
demonstrates a superior response and remission
rate then SRIs and that medication does not or in combination with SRIs showing strongest
increase the effectiveness of CBT. Regarding effects. It is important that treatment is
sustainability, the positive effects of CBT and approached in a developmentally appropriate
medication persist for years. One study on CBT manner that comprehensively addresses family
and SSRI for OCD in children and adolescents factors. These treatments have proven exception-
found that 85.3% of participants responded to ally efficacious. As a result, variations of treat-
treatment after 3-year follow-up (Melin et al., ment have emerged including brief CBT,
2018). CBT appears to have greater effectiveness parent-based treatment, and technology-assisted
than medication especially considering that the therapies. Although CBT with ERP has stood out
benefits of medication are attenuated if the medi- as the most well-supported approach for many
cation is stopped. CBT is recommended as the years, recent advances in understanding of expo-
first line of treatment, and medication alone sure mechanisms, the role of family in the pre-
should only be offered in the event that CBT is sentation and treatment of OCD, as well as
unavailable (AACAP, 2012). Taken together, technology-enhanced therapy have served to
meta-analyses show clear evidence for the effec- improve our understanding of how to optimize
tiveness of CBT and medication over waitlist and treatment outcomes for this population in recent
placebo control conditions in the treatment of years.
child and adolescent OCD; however, superior
effects are seen in CBT. Acknowledgment The authors report no relevant disclo-
sures for this chapter.
Summary
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Pharmacological Treatment
of Anxiety Disorders in Children 23
and Adolescents
Sohail Nibras, Anh Truong, and Laurel L. Williams
Introduction term. It is important to recognize that most SSRI

and SNRI medications are used “off-label” for
Anxiety disorders are the most common psychi- anxiety disorders. This term indicates that the
atric disorders in children and adolescents. specific medication is not FDA-approved even if
Among children aged 3–17 years, 7.1% have an another medication in the same class has shown
anxiety disorder, and the lifetime prevalence of efficacy in anxiety research trials. The FDA-
anxiety disorders is 31.9% in ages 13–18 approved medications are duloxetine, an SNRI,
(Ghandour et al., 2019). Evidence-based treat- approved for generalized anxiety disorder
ments include cognitive behavioral therapy (GAD), and the SSRIs fluoxetine, fluvoxamine,
(CBT) and two specific psychotropic medication and sertraline, approved for obsessive-compulsive
classes, the selective serotonin reuptake inhibi- disorder (OCD). In this chapter, we will explore
tors (SSRIs) and the serotonin norepinephrine medication classes frequently utilized for anxiety
reuptake inhibitors (SNRIs). The American disorders. Readers will note that the majority of
Association of Child and Adolescent Psychiatry medication use in youth anxiety disorders is off-
(AACAP) recommends CBT as the first-line label. The safety and efficacy of these medication
treatment for mild to moderate child and adoles- classes is the primary objective of this chapter.
cent anxiety without co-occurring mental health
disorders. For moderate to severe anxiety disor-
ders, the next level of intervention includes SSRIs elective Serotonin Reuptake
S
and possibly SNRIs (combined with CBT). In Inhibitors
areas with limited psychotherapy availability,
AACAP does recommend SSRI utilization as a Pharmacologic studies of childhood anxiety dis-
first-line intervention (Walter, 2020). orders have historically focused on the triad of
Rigorous clinical trial data indicate that the pediatric anxiety disorders comprised of general
combination of CBT and SSRIs may be more anxiety disorder (GAD), social phobia (SoP), and
effective than either treatment alone in the short separation anxiety disorder (SAD) to evaluate
pharmacologic interventions, as these diagnoses
S. Nibras (*) · A. Truong · L. L. Williams are commonly comorbid and share similar
Baylor College of Medicine, Menninger Department responses to pharmacologic treatments (Compton
of Psychiatry and Behavioral Sciences, et al., 2010). Of the psychopharmacologic inter-
Houston, TX, USA
e-mail: Sohail.Nibras@bcm.edu; altruong@bcm.edu; ventions, selective serotonin reuptake inhibitors
laurelw@bcm.edu (SSRIs) are the first-line treatment for this triad
https://doi.org/10.1007/978-3-031-14080-8_23
348 S. Nibras et al.
of anxiety disorders and have the most estab- et al., 2007). When comparing fluoxetine to clo-
lished efficacy for treatment of childhood anxiety mipramine and placebo, all three groups were
disorders through multiple randomized con- efficacious in treating anxiety disorders, with
trolled trials (Birmaher et al., 2003; March et al., fluoxetine showing the greatest response rate of
2007; Strawn et al., 2015; Wagner et al., 2004). 100%, compared to 87.5% and 77.7% for clo-
mipramine and placebo, respectively. Notably,
the placebo group in this study showed an unusu-
elective Serotonin Reuptake
S ally high response rate as compared to other stud-
Inhibitors’ Mechanism of Action ies (da Costa et al., 2013). Fluoxetine dosages in
these studies ranged from 10 mg daily to 60 mg
Selective serotonin reuptake inhibitors (SSRIs) daily (Beidel et al., 2007; Birmaher et al., 2003;
are the most commonly used medication to treat da Costa et al., 2013).
anxiety disorders in children, adolescents, and
adults. There are three common neurotransmit-
ters that are thought to affect the majority of psy- Sertraline
chiatric disorders. These are serotonin, dopamine,
and norepinephrine. These neurotransmitters are Sertraline has been found to be an effective treat-
thought to work by relaying neuronal messages ment for GAD, SoP, and SAD in multiple ran-
when released from synapses. These messages domized control trials. Rynn et al. found sertraline
lead to changes in gene transcription, and the to be more efficacious in the treatment of GAD
deficiency of these neurotransmitters is thought than placebo at a dose of 50 mg/day (Rynn et al.,
to result in mood and anxiety symptoms. 2001). The Child/Adolescent Anxiety Multimodal
Reuptake inhibitors such as SSRIs block mono- Study (CAMS), a landmark NIMH-funded multi-
amine transporters, resulting in an increase in center randomized controlled trial, examined the
neurotransmitters, and ultimately leading to efficacy of sertraline monotherapy, cognitive
downstream gene transcription and symptom behavioral therapy (CBT), sertraline and CBT
relief (Hirschfeld, 2000). combination, and placebo pill in 488 children and
adolescents between the ages of 7 and 17 years,
with moderate to severe GAD, SoP, and
ypes of Selective Serotonin
T SAD. Efficacy was measured by the Clinical
Reuptake Inhibitors Global Impression-Improvement (CGI-
Improvement) scale for clinical improvement and
Fluoxetine Pediatric Anxiety Rating Scale (PARS) for symp-
tom severity. The effect size was 0.86 for combi-
Multiple randomized controlled trials have found nation therapy, 0.45 for sertraline, and 0.31 for
that fluoxetine is an effective treatment for GAD, cognitive behavioral therapy. The CAMS conclu-
social phobia, and SAD (Beidel et al., 2007; sions were that combination of sertraline and
Birmaher et al., 2003; da Costa et al., 2013). CBT is more effective than either treatment alone
Birmaher et al. compared fluoxetine treatment to or placebo in reducing anxiety severity.
placebo and found that fluoxetine titrated up to Importantly, there was also no significant differ-
20 mg daily was more effective than placebo at ence between CBT and sertraline monotherapy
reducing anxiety symptoms and improving func- (Walkup et al., 2008). In the follow-up to the
tioning (61% vs. 35%) over 12 weeks of treat- CAMS trial, the Child/Adolescent Multimodal
ment. Fluoxetine was an effective treatment for Extended Long-Term Study (CAMELS) evalu-
social phobia when compared to Social ated 319 children for anxiety symptoms. Across
Effectiveness Training (SET-C) and placebo. all 4 years, 21.7% of youth were in stable remis-
However, SET-C was superior to both fluoxetine sion, 30% were chronically ill, and 48% relapsed.
and placebo for improving social skills (Beidel Those who responded initially to acute treatment
23 Pharmacological Treatment of Anxiety Disorders in Children and Adolescents 349
were more likely to be in remission at follow-up maximum dose of 40 mg/day over 12 weeks.
(Ginsburg et al., 2018). Functional outcomes They also received eight brief cognitive behav-
including global (i.e., life satisfaction) and ioral therapy-oriented counseling sessions lasting
domain-specific (i.e., social, familial, educa- 15 minutes each. On the CGI-Improvement scale,
tional/occupational, and legal) have also been about 83% of the participants reported “very
measured in CAMELS and showed that there much improved” symptoms and 41.7% reported
were meaningful long-term functional benefits in “much improved” symptoms of social and gener-
responders and remitters 3–12 years after treat- alized anxiety disorder. A small number of par-
ment (Swan et al., 2018). ticipants tolerated citalopram without any side
effects (Chavira & Stein, 2002).
Paroxetine
Escitalopram
There is only one randomized control trial which
evaluates the use of paroxetine in children and There are no pediatric anxiety disorders RCTs
adolescents with anxiety disorders, with social for escitalopram. Isolan et al. (2007) completed
phobia as their predominant psychiatric diagno- an open-label trial, in which they treated 20
ses. Wagner et al. (2004a) completed a multi- youths ages 10–17 with social anxiety disorder
center, double-blind, randomized controlled trial for 12 weeks using escitalopram. The dosage
treating 322 children and adolescents with a range was 2–20 mg/day. They found that 65%
diagnosis of social phobia with paroxetine to (13/20) were much to very much improved post-
evaluate its efficacy and tolerability with a flexi- treatment (Isolan et al. 2007). In a retrospective
ble dosing schedule of between 10 and 50 mg/ chart review, Coşkun and team (2012) observed
day or placebo for 16 weeks. Efficacy was defined 11 preschoolers (eight girls) with ages ranging
as being “much improved” or “very much from 47 to 64 months. Three participants showed
improved” on CGI-Improvement with 77% moderate to much improvement in anxiety
response in paroxetine group compared to 38% in symptoms. It is important to note that 45% expe-
placebo group with a mean dose of paroxetine of rienced behavioral disinhibition resulting in 27%
24.8 mg/day (Wagner et al., 2004a). Paroxetine dropping out of the study due to this side effect.
utilization for all pediatric psychiatric disorders The authors concluded that young children may
ceased in 2004 when the UK (United Kingdom) experience more side effects, particularly behav-
Medicine and Healthcare Products Regulatory ioral disinhibition (Coşkun et al., 2012).
Agency analysis indicated both a lack of efficacy
for major depression and an increase in suicidal
behavior in children. Fluvoxamine
Fluvoxamine is FDA approved for OCD only and

Citalopram commonly used in clinical setting treat anxiety.
The Research Units on Pediatric
There are no pediatric anxiety RCTs for citalo- Psychopharmacology (RUPP) Anxiety Study
pram, and only open trial level data are available. Group (2001) conducted a large-scale, random-
One 12-week open-label trial examined the cita- ized, placebo-controlled trial involving 128 pedi-
lopram’s efficacy for anxiety. Twelve children atric patients (ages 6–17) with multiple different
and adolescents from 8 to 17 years old partici- anxiety disorders including social phobia, sepa-
pated and two participants dropped out due to ration anxiety disorder, and generalized anxiety
side effects of nausea, lightheadedness, and con- disorder. These participants had received 3 weeks
centration problems. They received citalopram at of psychological treatment prior to the trial. The
a starting dose of 10 mg/day titrating up to a fluvoxamine dose was up to 300 mg/day.
Fluvoxamine was found to make a significant dif- day to 75 mg/day. The Social Anxiety Scale-
ference in CGI-Improvement and endpoint Child or Adolescent version (SAS-CA) and
Pediatric Anxiety Rating Scale (PARS) scores. CGI-I scores rated efficacy and responder assess-
Improvement in the fluvoxamine group was seen ment at each visit respectively. The safety proto-
in 48/63 participants (76%) compared to 19/65 col measured weight, heart rate, temperature, and
for the placebo group (29%) with P < 0.001. In electrocardiogram (EKG) during the visits. Due
general, fluvoxamine was well tolerated; to lack of efficacy (35%) and adverse effects, 4%
however, the youth had increased motor activity of youth discontinued the trial. Over a 16-week
and abdominal discomfort compared to placebo, period, the dose was titrated from 37.5 mg to a
17 (27%) vs. 8 (12%) and 31 (49%) vs. 18 (28%), maximum dose of 225 mg. Approximately 56%
respectively (Riddle et al., 2001). Following this of the participants in the venlafaxine ER group
trial, RUPP group investigated for pharmacologi- were rated much to very much improved on the
cal treatment moderators and mediators in pedi- CGI-Improvement scale compared to 37% in the
atric anxiety disorders. Study did not find any placebo group. Commonly reported side effects
mediators; however, analysis noted that subjects were asthenia (20% vs. 9%), anorexia (22% vs.
with social phobia (P < 0.05) and greater baseline 5%), nausea (23% vs. 11%), and weight loss
illness severity (P < 0.001) were less likely to (11% vs. 3%) during the treatment period. During
improve in either treatment group (RUPP Anxiety the titration phase, participants complained of
Study Group, 2002; Walkup et al., 2003). dizziness (13%), headaches (12%), nausea (7%),
and nervousness (6%). Additionally, three
patients developed suicidal ideation with no com-
Serotonin Norepinephrine pleted suicide, and one patient developed an epi-
Reuptake Inhibitors sode of hypomania with venlafaxine ER. The
study concluded that venlafaxine ER is well tol-
Venlafaxine erated and an effective treatment for children and
adolescents with generalized social anxiety dis-
Venlafaxine is an SNRI whose mechanism of order (March et al., 2007).
action is to increase the availability of serotonin
and norepinephrine. Although it is FDA-approved
for GAD and social anxiety disorder in adults, it is Duloxetine
not currently FDA-approved for pediatric patients.
In an 8-week, placebo-controlled RCT for youth Duloxetine is a serotonin and norepinephrine
ages 6–17 with GAD, Ryan and colleagues found reuptake inhibitor (SNRI). It is the only antide-
venlafaxine XR improved both GAD symptoms pressant FDA-approved for pediatric GAD.
and HAM-A score compared to placebo (69% vs. Strawn and colleagues conducted an RCT with
48%; P < 0.001). Although venlafaxine was rela- flexible dosing for 10 weeks in the acute phase,
tively well tolerated compared to placebo, partici- continuing afterward for 18 weeks of open-label
pants experienced the following adverse reactions: duloxetine treatment in 272 youth. Participant
anorexia (13% vs. 3%), pain (17% in both groups), ranged from 7 to 17 years old with a primary
somnolence (11% vs. 0%), weight loss (5% vs. diagnosis of GAD. Duloxetine was superior to
1%), as well as changes in blood pressure (3.25% placebo in symptomatic response (50% improve-
vs. 1.6%), pulse, cholesterol level, and height ment on PARS severity for GAD; P < 0.001,
(Ryan et al., 2007). remission (PARS severity for GAD ≤ 8), and
In a 16-week, placebo-controlled RCT, 293 functional remission (CGAS >70; P < 0.05). In
participants ages 8–17 across 48 academic and the duloxetine group, adverse effects of systolic
community centers with a diagnosis of separation blood pressure changes, heart rate changes, and
anxiety disorder participated in a venlafaxine ER minor weight loss were observed (Strawn et al.,
trial. Venlafaxine ER dose ranged from 37.5 mg/ 2015).
Benzodiazepines to establish efficacy or safety of buspirone for the

treatment of anxiety disorders in the pediatric
Benzodiazepines are drugs that enhance the population. Two unpublished trials consisting of
effects of the neurotransmitter gamma-two placebo-controlled 6-week trials involving
aminobutyric acid (GABA) at the GABAA recep- 559 pediatric patients, ages 6–17 years, with
tor leading to sedative, hypnotic, anticonvulsant, GAD (dosing 15–60 mg/day) found no signifi-
and anxiolytic properties. They have a rapid onset cant difference between buspirone and placebo.
of action leading to relief of anxiety symptoms Strawn et al. (Strawn et al., 2018a) completed an
within minutes to hours. While benzodiazepines analysis of these abandoned studies and con-
have been supported by research for the treat- firmed that buspirone did not differentiate from
ment of adult anxiety disorders, there is limited placebo, but posited that the studies were under-
research on the use of benzodiazepines in the powered to identify small differences, thus no
pediatric population (Ballenger et al., 1988). To firm conclusions can be made about the utility of
date, only two randomized clinical trials have buspirone in children and adolescents (Strawn
evaluated benzodiazepines for treatment of ado- et al., 2018a).
lescent anxiety disorders (Graae et al., 1994;
Simeon et al., 1992). In youth of ages 7–13 with
SoP and GAD who were treated with clonaze- Guanfacine
pam, there was no significant difference between
clonazepam and placebo (Graae et al., 1994). Guanfacine is approved to treat attention deficit
Evaluation of alprazolam compared to placebo in hyperactivity disorder (ADHD) in children and
youth with GAD, ages 8–17, showed similar adolescents. It acts by stimulating post-synaptic
results, with no significant difference in anxiety alpha-2 adrenergic receptors resulting in down-
symptoms found between alprazolam-treated and stream effects on the prefrontal cortex, an area of
placebo-treated youth (Simeon et al., 1992). Poor the brain associated with learning and memory.
response to benzodiazepine treatment in adoles- While it is unclear how guanfacine may mediate
cents with anxiety disorders is particularly anxiety symptoms, a pilot study by Strawn et al.
important to note, especially in adolescents with evaluated the safety, tolerability, and potential
a history of substance abuse, as the potential for anxiolytic efficacy of guanfacine in children and
benzodiazepine abuse, addiction, and diversion adolescents with GAD, SoP, and SAD and found
must be considered. guanfacine was associated with greater improve-
ment in CGI-Improvement scores compared to
placebo (54.2% vs. 31.6%). However, no
Medications for Treatment improvement was noted on measures of anxiety,
Augmentation Pediatric Anxiety Rating Scale (PARS), and
Screen for Child Anxiety Related Disorders
Buspirone (SCARED) scores. Guanfacine was dosed
between 1 and 6 mg daily and overall was well
Buspirone represents a unique class of anxiolyt- tolerated (Jeffrey R Strawn et al., 2017).
ics and is a serotonin-1A (5-HT1A) receptor par-
tial agonist. Though its mechanism of action is
not fully understood, it is suspected that the par- Hydroxyzine
tial 5-HT1A agonism translates into increased
serotonergic activity in the amygdala and other Hydroxyzine belongs to the class of antihista-
parts of the brain’s fear and anxiety circuit result- mines that includes such medications as diphen-
ing in a reduction in anxiety (Jann, 1988). hydramine. It acts on the histamine-1 (H1)
Buspirone is mildly efficacious for treatment of receptor and antagonizes muscarinic receptors
adult anxiety disorders, but there is limited data and 5-HT2A receptors, which is thought to help
with anxiety. It is approved by the FDA for adult (N = 60). The dose of clomipramine ranged from
anxiety; however, in the clinical setting, its use is 75 mg/day to 150 mg/day for weights 25–30 kg
limited to anxiety presenting in a medical setting to >60 kg. Subjects in clomipramine group had
with organic diseases or medical procedures. As 37% mean reduction in symptoms on the Y-BOCS
with other antihistamines, it may cause sedation, (p < 0.05) compared to 8% in placebo group
fatigue, dizziness, dry mouth, increased appetite, (DeVeaugh-Geiss et al., 1992).
and constipation and for youth, a paradoxical
hyperactive response (Connolly, 2007; Patel
et al., 2018). Administration, Monitoring,
and Discontinuation
Tricyclic Antidepressants (TCAs) Selecting medications for treatment of child and

adolescent anxiety disorders is based upon mul-
Since the introduction of SSRIs in the 1980s, the tiple factors including age, psychiatric and medi-
use of TCAs has declined as mainstay psycho- cal comorbidities, family history of treatment
pharmacology. There are two categories of TCAs: response, side effect profiles, potential for treat-
tertiary amines and secondary amines. Tertiary ment non-adherence, and patient and family pref-
amines include amitriptyline, clomipramine, erence. In general, medications should be started
doxepin, imipramine, and trimipramine. at the lowest possible dose and increased based
Secondary amines include desipramine, nortrip- on clinical efficacy. Antidepressants dosing is not
tyline, and protriptyline. Tertiary amines are weight-based in children and adolescents. While
potent serotonin inhibitors and secondarily are antidepressant medications may take up to
effective norepinephrine blockers (Strawn et al., 6–8 weeks to reach maximum effectiveness, a
2018a). Due to cardiac adverse effects and the response may be noted within 2 weeks (Strawn
availability of alternatives with better safety pro- et al., 2018b; Varigonda et al., 2015). If there is
files (SSRIs and SNRIs), there has been a decline no improvement in symptoms, medication dos-
in TCA utilization across clinical settings. Klein ages should be increased or changed depending
and colleagues investigated the efficacy of imip- on medication tolerability. According to the
ramine in children (n = 21) with separation anxi- Federal Drug Administration (FDA), monitoring
ety disorder. This 6-week placebo-controlled should be weekly for the first 4 weeks after initia-
RCT found that imipramine was not superior to tion, biweekly in the second month, and monthly
placebo. The imipramine group had moderate to thereafter. There are several self-report measures
severe side effects including irritability and to screen for anxiety disorders in children and
anger. Da Costa and colleagues’ double-blind, adolescents including the Revised Children’s
placebo-controlled RCT of clomipramine (n = 9), Manifest Anxiety Scale (RCMAS),
fluoxetine (n = 10), and placebo (n = 11) for Multidimensional Anxiety Scale for Children
12 weeks concluded that clomipramine showed (MASC), and the Screen for Child Anxiety
similar efficacy in the comparisons of CGI and Related Disorders (SCARED). Both the MASC
C-GAS: CGI (placebo, p < 0.001, clomipramine, and SCARED have adolescent and parent rating
p = 0.001, fluoxetine, p < 0.001) compared with versions and may help monitor treatment prog-
fluoxetine but, importantly, was not superior to ress (Birmaher et al., 1999; Lee et al., 1988;
placebo (da Costa et al., 2013). Previously litera- March et al., 1997).
ture has shown clomipramine to be effective for Discontinuation of medications should be
obsessive compulsive disorder (OCD). OCD was considered after 8–12 months of remission from
previously listed under anxiety disorders in DSM anxiety symptoms, ideally during a time of low
IV-TR. DeVeaugh-Geiss et al. (1992) in an stress and over several weeks monitoring for a
8-week multisite study found clomipramine to be return of symptoms or side effects to
effective in children and adolescent with OCD discontinuation.
afety, Adverse Effects,

S sufficient evidence of efficacy for pediatric anxi-
and the Blackbox Warning ety disorders or symptoms. Physicians should
provide families and youth with psychoeducation
SSRIs are the most commonly used first-line related to side effects of SSRI and SNRIs, as dis-
medications for anxiety disorders. Dobson and continuation of treatment is high in pediatric
colleagues in 2019 conducted a meta-analysis to anxiety trials. Additionally, physicians should
evaluate the efficacy and tolerability of pediatric educate families on the FDA Suicide Warning
psychopharmacology for anxiety disorders. They while simultaneously monitoring for suicidal ide-
concluded that SSRIs are superior to SNRIs, ations or behaviors especially in the initial phases
which are superior to 5-HT1A agonists and TCAs of treatment. The SSRIs and SNRIs can be the
in terms of tolerability. SSRIs and TCAs were initial treatment option for moderate to severe
better tolerated compared to alpha-2 agonists. anxiety or in mild cases where CBT availability
Overall, SSRIs are superior for reducing anxiety is limited. The combination of CBT and SSRIs is
in the pediatric population, but due to adverse more effective than either treatment alone.
effects, the likelihood of discontinuation is high
without proper titration and management of
expectations (Dobson et al., 2019). It is important References
to share with caregivers and patients that the fol-
lowing are common side effects and are generally Ballenger, J. C., Burrows, G. D., DuPont, R. L., Lesser,
I. M., Noyes, R., Pecknold, J. C., et al. (1988).
both mild and transient: nausea, vomiting, diar- Alprazolam in panic disorder and agoraphobia:
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A Common Mechanism for Anxiety
Disorders and Drug Addiction: 24
Implications for Current and Novel
Pharmacological Treatments
Marco A. Grados and Bushra Rizwan
Pharmacological treatments of anxiety in adoles- substance abuse is a “secondary” disorder is gen-

cents generally follow the same guidelines as erally prevalent (Kushner et al., 1990). Often the
treatment of anxiety in adults. In order to provide “primary” disorder is considered as that which
a working framework that considers the dual appears first, yet this presentation may develop as
diagnosis of anxiety disorder and substance a function of environmental exposures or triggers
abuse, a biological perspective on anxiety and rather than clinical or biological predominance.
substance abuse is presented with a focus on a A different approach might consider that biologi-
common mechanism of conditioned responses cal pathways in common may predispose patients
resulting in a shared pathophysiology. to both conditions.
Implications for treatment approaches are then From an epidemiological perspective, anxiety
considered. and substance use disorders are among the most
prevalent psychiatric disorders, with lifetime
rates of 28.8% and 14.6%, respectively (Kessler
Phenomenology of Anxiety et al., 2005). Further, if generalized anxiety dis-
Disorders and Substance Abuse order or panic disorder are present, then odd ratio
(confidence interval) for substance dependence is
Anxiety and substance use disorders coexist 9.5 (4.8–18.8), lower for social phobia 4.5 (2.5–
more frequently than expected by chance in both 8.2) and specific phobia 3.8 (2.1–6.7). In addi-
the general population and clinical samples tion, post-traumatic stress disorder (PTSD) has
(Castle, 2008). As occurs when psychiatric con- been shown to correlate strongly with alcohol use
ditions co-occur, for dual diagnosis patients it is disorder (Compton et al., 2007). Up to 50% of
not always possible, or even heuristic, to deter- individuals seeking treatment for substance
mine which disorder is “primary” and which is dependence have a comorbid anxiety disorder
“secondary.” Notwithstanding, the notion that (Kushner et al., 1990), with implications for
treatment as well as recovery. Thus, while it is
biologically plausible that substance use disor-
M. A. Grados (*) ders, including alcohol abuse, may uncover sus-
Johns Hopkins University School of Medicine, ceptibilities to anxiety disorders as evidenced by
Baltimore, MD, USA
e-mail: mjgrados@jhmi.edu experiments showing that alcohol cues activate
brain regions associated with negative affect
B. Rizwan
Kennedy Krieger Institute, Johns Hopkins University (Feldstein et al., 2009), it is also plausible that
School of Medicine, Baltimore, MD, USA alcohol and substance use diminish the threshold
https://doi.org/10.1007/978-3-031-14080-8_24
358 M. A. Grados and B. Rizwan
for clinical anxiety symptom expression ally framed as a conditioned response or learned
(Feldstein et al., 2009). For example, ethanol and behavior. Rat studies support the notion that, as
corticotropin releasing factor (CRF) interact to conditioned responses, both anxiety and drug-
increase release of GABA in central amygdalar seeking are subsumed by initiation in prelimbic
nuclei, setting the stage for increased anxiety cortex circuitry and suppression circuitry in
expression in relation to alcohol consumptpion infralimbic cortex (Peters et al., 2009). In this
(Roberto et al., 2020). Additionally, individuals physiologic framework, the infralimbic rat brain
with comorbid alcohol abuse and anxiety disor- region is analogous to human ventral prefrontal
ders are at higher risk for relapse after alcohol cortex (Brodmann Areas 10–13, Brodmann Area
treatment, with social phobia predicting any 25), a critical brain region involved in emotional
relapse and panic disorder predicting dependence regulation and ultimately responsible for sup-
relapse (Kushner et al., 2005). Other studies have pression of (adaptive or maladaptive) conditioned
reaffirmed the importance of taking into consid- responding (Peters et al., 2008). Extinction mem-
eration co-occurring depressive and anxiety dis- ory, a process that involves the suppression of
orders when treating individuals for substance conditioned responses, serves to regulate the
use, with a significant impact on long-term dis- emotional response to learned behaviors.
ability (Bovasso, 2001). Further, there is epide- Stimulation of the infralimbic area in rats, both
miologic support for a common “factor” electrophysiologically (Milad & Quirk, 2002)
underlying both psychiatric and substance abuse and pharmacologically (Sierra-Mercado Jr. et al.,
morbidity. In a study of over 5000 respondents to 2006), are associated with stronger extinction
a questionnaire on depressive, anxiety, alcohol, memory learning. The same stimulation is now
and drug use disorders, there was significant associated with enhanced regulation of emotional
familial aggregation among disorders. That is, if responses to learned behaviors, aiding behavioral
the proband had one of the disorders, then rela- extinction. For example, in Sierra-Mercado Jr.
tives were more likely to have the other disorders et al. (2006), tetrodotoxin inactivated the ventro-
even if the relative did not have the original pro- medial prefrontal cortex in rats prior to extinc-
band disorder (Kendler et al., 1997). tion, which led to impaired recall of extinction
the next day. These data suggest that active
extinction-related neuroplasticity in targeted
Pathophysiology of Anxiety brain areas plays a role in fear extinction. These
Disorders and Substance Use same areas could then subsume learned behav-
iors for anxiety conditioning as well as the inabil-
Anxiety disorders and substance use can be ity to regulate emotional responses in
framed in the context of conditioned responses, drug-seeking behaviors. The amygdala, in par-
anxious or appetitive, respectively. Anxiety can ticular, is thought to be involved in all stages of
be partly understood as a conditioned or learned fear learning, but prefrontal areas are specific to
fear response, building on an inborn reactivity to the extinction phase (Delgado et al., 2006). In
threatening stimuli, captured under the concept particular, long-term potentiation (LTP) mainte-
of “fear conditioning.” Key brain areas underly- nance in the medial prefrontal cortex is associ-
ing fear conditioning include the amygdala and ated with maintenance of extinction learning,
insula. Subjects with social and specific phobias preventing a return of a fear response after
and healthy subjects undergoing fear condition- administration of the conditioned fear-inducing
ing, for example, have consistently shown greater stimulus in mice (Herry & Garcia, 2002). Using a
amygdala and insula activity associated with similar paradigm, it has been proposed that
negative emotional responses compared to extinction failure in the appetitive domain can
matched comparison subjects (Etkin & Wager, lead to relapse in addiction. Studies now show
2007). Substance use disorders, operationalized that by inhibiting select brain nuclei with GABA
as drug-seeking behaviors, can also be conceptu- agonists, suppression of cocaine-seeking pro-
24 A Common Mechanism for Anxiety Disorders and Drug Addiction: Implications for Current and Novel… 359
duced by previous extinction training requires est that DCS has been effective when used acutely
activity in the rat infralimbic cortex (Peters et al., shortly before (Walker et al., 2002) or immedi-
2008). On the contrary, activating the same brain ately after (Ledgerwood et al., 2005) extinction
region with glutamate-based AMPA receptor sessions; more chronic use of DCS can have a
stimulation, reinstatement of cocaine drug- blunting effect on the beneficial effects of imme-
seeking was suppressed in these animals (Peters diate DCS (Quartermain et al., 1994). However,
et al., 2008). As noted above, the infralimbic cor- subsequent studies were unable to reproduce
tex also subsumes extinction learning in anxiety- these findings (Ori et al., 2015).
based paradigms. In contrast to anxiety-based The management of stress, in turn, has been
circuitry, in drug addiction, the connection of the linked to improving outcomes in relapse preven-
infralimbic cortex to the nucleus acccumbens tion in substance abuse (Goeders, 2003). A physi-
(NAc) shell plays a critical role. Inhibition of the ologic connection between exposure to stress,
NAc shell induces cocaine-seeking in rats with modifications of the hypothalamic–pituitary–
prior extinction training (Sesack et al., 1989). adrenal (HPA) axis, and abstinence cravings sug-
gest such an approach. In animals, exposure to
electric footshock increases subsequent reinforc-
Principles of Treatment of Anxiety ing efficacy of heroin (Shaham & Stewart, 1994)
Disorders and Substance Use and morphine (Will et al., 1998). Thus, it is not
surprising that the acquisition of amphetamine
In concert with the parallel pathophysiology of and cocaine self-administration is enhanced in
anxiety and substance abuse based on plausible rats exposed to tail pinch (Piazza et al., 1990),
common biological substrates for conditioned social defeat (Kabbaj et al., 2001), or neonatal
learning, there are similarly possible common isolation (Kosten et al., 2000), all stress-inducing
approaches to conceptualizing interventions that environmental conditions. By activating the HPA
aim to provoke extinction memory or suppres- axis, it is plausible that anxiety disorders gener-
sion of conditioned responses for both anxiety ate a persistent internal milieu that is analogous
disorders and drug addiction. The amygdala to the effects of outward adverse environmental
plays a role in modulating anxiety extinction stressors. Additionally, anxiety disorders precipi-
memory via the lateral nucleus (LA), the afferent tated by environmental stressors may similarly
arm of the amygdala which receives input from mediate the effects of the adverse environment
the cortex and thalamus. The LA dissipates its and perpetuate its effect. In both cases, environ-
neuronal firing in cell experiments if the uncondi- mental stressors, anxiety disorders, and substance
tioned stimulus (UCS), for example an electric abuse become intertwined in a self-perpetuating
shock, following the conditioned stimulus (CS) cycle of relapse and barriers to effective treat-
sound, is no longer delivered after the CS on mul- ment. Given that childhood anxiety disorders are
tiple occasions (Quirk et al., 1995). An important precursors to later mental health vulnerabilities,
goal of clinical intervention in anxiety disorders early intervention in anxiety disorders could
is to facilitate extinction of fear responses through plausibly address a critical link in the longitudi-
exposure. Any adjuvants to extinction learning nal acquisition of later co-occurring conditions in
thus enhance the therapeutic process. Facilitation different environmental contexts.
of neuroplasticity in the amygdala for learning of Given the plausible etiological connections
extinction responses may then be germane to between stress, anxiety, and substance abuse, it is
enhancing anxiety treatments (Myers & Davis, not surprising that, in particular, post-traumatic
2002). In this way, the use of D-cycloserine stress disorder (PTSD) has been associated with
(DCS), a partial glutamate agonist, has been used substance abuse. Psychopathologically, PTSD is
to facilitate extinction learning and has proven to a multi-determined clinical condition, mediated
even prevent learned fear after reinstatement of by the environmental exposure in vulnerable
the UCS (Ledgerwood et al., 2004). It is of inter- individuals. Females with a history of affective
disorders are at higher risk for PTSD while males et al., 2003), which are in turn highly comorbid
with a history of anxiety disorders are similarly at with alcohol abuse (Saraceno et al., 2009).
higher risk (Bromet et al., 1998). In turn, indi-
viduals who are engaged in substance abuse are
at increased risk for exposure to trauma (Cottler harmacology in Anxiety Disorders
P
et al., 1992). In this complex interaction between and Substance Abuse: Current
anxiety, PTSD, substance abuse, and exposure to and Novel Approaches
trauma, it appears that anxiety disorders mostly
precede PTSD but that subsequent occurrence of While psychosocial treatments for substance use
PTSD or multiple traumas does not increase the disorders are a primary intervention to break the
occurrence of other anxiety disorders; therefore, cycle of drug use and drug-seeking behaviors, the
non-PTSD anxiety disorders appear to act pri- current focus will be on the pharmacological
marily as predisposing factors for both PTSD and treatment of anxiety disorders in the context of
substance abuse. In a comprehensive study of substance use in adolescents. Most trials of anti-
1420 children followed longitudinally, traumatic anxiety agents do not include individuals with
events were fairly common and did not frequently substance use, as this is almost universally an
result in PTSD; however, multiple traumas or exclusion criterion in efficacy trials. Therefore,
prior anxiety disorders were associated with informed but empirical clinical decision-making
PTSD development (Copeland et al., 2007). In needs to guide treatment approaches, given the
another study of 1140 children in South Africa, a paucity of controlled data in dual diagnosis popu-
clear relationship was found between cumulative lations, especially adolescents. Alcohol with-
trauma and incidence of PTSD symptoms and drawal, for example, uniformly causes anxiety
depression but not of anxiety disorders (Suliman and benefits from anxiety pharmacologic man-
et al., 2009). In particular, the subgroup of chil- agement strategies, but also from medications
dren who are poly-victimized (Finkelhor et al., such as naltrexone to reduce cravings, which is
2009) are thus at high risk for both PTSD and not used in primary anxiety disorders.
substance abuse. Childhood abuse is associated In adults, alcohol-related depression has
with a persistent sensitization of the HPA axis in shown a good response to selective serotonin
adulthood, and in children, a similar sensitization reuptake inhibitor (SSRI) treatment (Lejoyeux,
has been detected in social anxiety patients with 1996). And in general, given the wide spectrum
a history of childhood abuse (Elzinga et al., of anxiety disorders that respond to SSRIs, this
2009). medication class remains the treatment of choice
In light of the plausible influence of pediatric for anxiety in the context of comorbidity, includ-
anxiety disorders on the development of sub- ing substance use disorders (Dunner, 2001). As
stance abuse, an epidemiologic perspective evidenced by studies in adults, SSRIs can also be
would strongly support the early treatment of helpful in the context of alcoholism comorbid
anxiety, especially in vulnerable children (i.e., with PTSD (Brady et al., 1995) as well as social
positive family history of substance abuse, expo- anxiety (Randall et al., 2001). SSRIs are also
sure to trauma). While much research is sorely generally safe in the context of medical compli-
needed to establish reciprocal etiological path- cations from substance abuse, such as liver dys-
ways between anxiety and substance use disor- function (see Table 24.1). On the other hand,
ders, there is sufficient evidence to recommend bupropion (Wellbutrin) is not recommended in
the early detection and treatment of anxiety in patients with co-occurring affective disorders and
childhood as a component of a general strategy to alcohol use disorder, due to a potential to decrease
prevent distal substance use disorders, depres- the seizure threshold and higher risk of alcoholic
sion, and PTSD outcomes. In particular, it is withdrawal seizures (Silverstone et al., 2008).
known that early-life anxiety disorders predis- Buspirone (Buspar) has been used to control
pose to adult anxiety disorders (Kim-Cohen anxiety symptoms in alcohol abuse with reduced
Table 24.1 Sample pharmacologic approaches to treatment of comorbid anxiety and substance abuse
Drug Use Side effects Comments
Conventional pharmacological approaches
SSRIsa (Fluoxetine) Ethanol Insomnia, headaches, GI upset, sexual Broad spectrum use for anxiety
(20–40 mg/day or abuse or dysfunction and depressive disorders
equivalent; single drug abuse associated with dual diagnosis
dose)
Buspirone (Buspar) Ethanol Dizziness, nausea, headache, Anxiolytic properties useful in
(15–60 mg/day; abuse or nervousness, lightheadedness ethanol/opioid abuse
divided doses) opioid
abuse
Novel pharmacological approaches
Gabapentin Ethanol Back pain, diplopia or blurry vision, Animal studies suggest specific
(Neurontin) (300– abuse clumsiness, constipation, diarrhea, effect in ethanol-dependence; may
1800 mg/day; divided dizziness, drowsiness, dry mouth, also decrease withdrawal-
doses) nausea, stomach upset, tiredness, associated anxiety from ethanol
vomiting, weight gain and cocaine
N-acetylcysteine Cocaine Nausea, vomiting, headache, rash, dry Pretreatment with
(200–1200 mg/day) abuse mouth, dizziness, or abdominal pain N-acetylcysteine prevents
(cramps, diarrhea), depletion heavy cocaine-induced changes in
metals and vitamins nucleus accumbens
a
Selective serotonin reuptake inhibitors: fluoxetine (Prozac), sertraline (Zoloft), fluvoxamine (Luvox), escitalopram
(Lexapro), citalopram (Celexa), paroxetine (Paxil)
anxiety and drinking associated with its use transmission was attenuated. Gabapentin pro-
(Kranzler et al., 1994). A similar positive experi- duces a different effect in nondependent rats, spe-
ence was obtained with the use of buspirone in cifically, an increase in GABA transmission
methadone patients (McRae et al., 2004). By (Roberto et al., 2008). Thus, gabapentin may
extension, these approaches may be reasonable in have a specific use in the context of ethanol
adolescent populations that require pharmaco- dependence separate from that in non-dual diag-
logical management of anxiety disorders in the nosis patient. Further, in experimental animals,
context of alcohol abuse or opioid dependence. anxiety-related withdrawal was attenuated with
The benzodiazepine class of medications are gapapentin, which suggests that relief of anxiety
not a favorable option for comorbid anxiety dis- via GABA mechanisms may attenuate alcohol
order and substance use disorder due to higher consumption. Gabapentin is thus a promising
potential for misuse, but they can be instrumental drug for treating alcohol abuse via its anxiolytic
in alcohol withdrawal protocols. The use of properties (Clemens & Vendruscolo, 2008).
GABAergic agents for managing drug depen- Earlier, gabapentin had been used to treat cocaine
dence focuses on reducing cravings, making use craving in 30 cocaine-dependent subjects. In an
of glutamate–GABA brain homeostasis modula- 8-week, open-label trial of 1200 mg/day of gaba-
tion. Gabapentin (Neurontin), a non-pentin, there was a very significant reduction in
benzodiazepine anticonvulsant GABA analog, craving and use of cocaine in the treated group
modulates transmission in the central amygdala (Myrick et al., 2001). Pregabalin (Lyrica) is
(CeA) via GABA-B receptors (Roberto et al., structurally similar to gabapentin but more potent
2008). Ethanol, also modulates GABAergic as a GABA analogue (Wensel et al., 2012) and
transmission in the pre- and post-synapse in the can be considered for similar uses. Although
CeA, but apparently via GABA-A receptors GABAergic medication use has been promising,
(Roberto et al., 2003). More importantly, when to date, several experimental GABA-A receptor
ethanol-dependent rats, which developed an subtype agonists have failed to reach the market
increase in baseline GABA transmission were due to poor efficacy and tolerability (Griebel &
administered gabapentin, the excess GABA Holmes, 2013).
In the last decade, clinical research had provide initial evidence for a putative common
explored modulation of glutamate NMDA recep- mechanism for anxiety and substance use disor-
tors as a potential target. In this context, drugs ders, in particular, early treatment of anxiety
that were NMDA receptor antagonists block emerges as a potential preventative measure to
extinction and reconsolidation of fear memories. avert later substance use disorders. If these obser-
CNS glutamate modulators are glycine and vations are supported by future research, there
D-serine (agonists), felbamate (antagonist), and will be a notable opportunity to develop pharma-
D-cycloserine (partial agonist). Ketamine, aman- cological treatments that take advantage of shared
tadine, memantine, dextromethorphan, and rilu- biological mechanisms, mostly focused on the
zole are glutamate modulators, with potential for CNS glutamate–GABA homeostatic system.
improving GABA–glutamate homeostasis; how-
ever, due to multiple receptor targets and mecha-
nisms, these drugs are only initially being used to References
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Part IV
Food Neophobia in Children:
Misnomer, Anxious Arousal, 25
or Other Emotional Avoidance?
Dean McKay and Charlene Minaya
The vital importance of nutrition and the severe

risks of poisoning may together account for the 2003; Martins & Pliner, 2005; Milton, 1993;
strong affective responses associated with eating
and for the ambivalence associated with this pro- Russell & Worsley, 2008). In humans, the latter,
cess. This conflict… is represented by opposing protective mechanism appears to be especially
tendencies to fear and to explore new foods, or to pronounced in early childhood. When infants
like both familiar and novel foods. (Rozin & gain the capacity for locomotion, their diets
Fallon, 1987, p. 27)
become increasingly omnivorous and varied, and
Coined the “omnivore’s dilemma” (Rozin & an exclusive milk diet no longer provides ade-
Fallon, 1987), this evolutionarily based mecha- quate nutrition (Addessi et al., 2005; Cooke et al.,
nism, which is characterized by seemingly con- 2003; Dovey et al., 2008; Lafraire et al., 2016).
flicting inclinations to ingest and avoid unfamiliar Interestingly, infant rejection of novel foods can
foods, is thought to influence the food prefer- predict food neophobia in early childhood
ences and consumption of humans and other (Moding & Stifter, 2016a). The impact of food
omnivorous species (Addessi et al., 2005; Alley neophobia decreases dramatically in later child-
& Potter, 2011; Birch et al., 1998; Dovey et al., hood and continues to lessen at a more gradual
2008; Martins & Pliner, 2005; Rozin & Fallon, pace in adolescence and adulthood (Alley &
1987; Rozin & Vollmecke, 1986). Theoretically, Potter, 2011; Dovey et al., 2008).
the coexistence of food neophilia (approach to
new and unique foods) and food neophobia
(avoidance of unfamiliar or novel food items) Defining Food Neophobia
served to increase the probability that our early
ancestors sought and consumed foods that pro- Food neophobia has been operationally defined
vided adequate nutrition, while avoiding poten- as the rejection and avoidance of novel foods
tially poisonous or toxic plants, animals, and (Cooke et al., 2006; Dovey et al., 2008; Knaapila
animal products (Dovey et al., 2008; Flight et al., et al., 2007; Pliner & Hobden, 1992) and has
been conceptualized as both a behavioral process
and a personality trait (Pliner & Hobden, 1992).
D. McKay (*) In their seminal paper, Pliner and Hobden
Institute for Cognitive Behavioral Therapy and describe the food neophobia trait as “a continuum
Research, White Plains, NY, USA
along which people can be located in terms of
Fordham University, Bronx, NY, USA their stable propensity to approach or avoid novel
foods” (1992, p. 107). In order to highlight the
C. Minaya specificity of the food neophobia construct, sev-
Fordham University, Bronx, NY, USA
https://doi.org/10.1007/978-3-031-14080-8_25
368 D. McKay and C. Minaya
eral researchers have drawn attention to the dis- the child ultimately tries the food without undue
tinction between food neophobia and the more additional pressure.
general construct, picky eating, which is the gen- While past literature has focused largely on
eral reluctance to consume foods that are sensory hypersensitivity as a predictor, with
appraised as objectionable (Cooke et al., 2006; moderating effects based on parental eating hab-
Dovey et al., 2008; Galloway et al., 2003; Jacobi its, there is limited detailed evaluation of food
et al., 2003). Thus, food neophobia is considered neophobia and its treatment. The purpose of this
to be a subtype of picky eating characterized by chapter is to cover the existing literature, its asso-
unwillingness to consume unfamiliar foodstuffs ciation with different childhood psychological
(Dovey et al., 2008). conditions, and some potentially promising ave-
Avoidance of unfamiliar foods is an age-old nues for treatment. As the literature for this prob-
problem and is a common complaint among par- lem remains limited, we present illustrative cases
ents. They describe their children, who have where different levels of food aversion were pres-
highly restrictive diets, as “picky eaters.” A wide ent and how treatment was conceptualized. We
array of explanations have been offered for this recognize that this in no way represents a com-
pattern of avoidance in children, ranging from prehensive means of developing treatment guide-
increased taste sensitivity in youth (Cowart, lines for mental health practitioners but, instead,
1981) to a more recent conceptualization based suggests potential avenues for further
on global sensory hyperawareness (Coulthard & investigation.
Blissett, 2009; Mustonen & Tuorila, 2010) with
moderating effects based on mother’s food pref-
erences both pre- and postnatally. This has cre- athological Patterns of Food
P
ated difficulties in conceptualization of food Neophobia and Associated
neophobia in extreme cases, whereby dietary Consequences
restrictions lead to dietary deficits. Social facili-
tation can decrease food neophobia in youth, In contradistinction to the other diagnostic enti-
although this varies depending on the other per- ties outlined in this volume, comparatively little
son’s social status or role. Peer modeling can sig- research has been devoted to investigating the
nificantly decrease food neophobia, while relationship between normative and more mal-
parental modeling has shown little to no demon- adaptive patterns of food neophobia. Indeed, the
strable impact on decreasing food neophobia phenomenology, etiology, maintenance, and
(Kutbi et al., 2019; Lafraire et al., 2016). emotional underpinnings of food neophobia are,
Furthermore, parents may inadvertently worsen by and large, not well understood. What is clear,
the problem associated with food neophobia by however, is that a large minority of children and
pressurizing children to try unfamiliar foods that adolescents exhibit levels of food neophobia that
they make efforts to avoid (Moding & Stifter, constrain food selection to such a degree that diet
2016b). Tuorila and Mustonen (2010) conducted variety, diversity, and overall quality are nega-
an experiment with children who had food aver- tively impacted (Cooke et al., 2006, 2003;
sions (but not dietary deficits associated with the Falciglia et al., 2000; Galloway et al., 2003;
avoidance). A total of 72 children between ages 8 Russell & Worsley, 2008). Recent research sug-
and 11 years were given rating tasks for a range gests, however, that food neophobia has not dem-
of foods. The most negative ratings were given to onstrated a clear, direct association with
foods that the children (a) expressed a reluctance childhood weight status (Brown et al., 2016; Tan
to try even though they had never had those & Holub, 2012). Kaar et al. (2016) found that
foods, and (b) were nevertheless pressed to try. food neophobia and overweight status were
This suggests that efforts to induce trying of new linked through decreased vegetable consumption
foods require additional inducements whereby and additional research has pointed to a negative
25 Food Neophobia in Children: Misnomer, Anxious Arousal, or Other Emotional Avoidance? 369
relationship between food neophobia and vegeta- Falciglia et al. (2000) compared the diets of
ble consumption (Proserpio et al., 2020). Further, fourth- and fifth-grade students with varying lev-
picky eating in childhood has been demonstrated els of food neophobia. Participants were classi-
to increase the risk of developing extreme levels fied into one of three groups based on their scores
of anorexic symptoms in adolescence (Marchi & on the Food Neophobia Scale (Pliner & Hobden,
Cohen, 1990). 1992): (a) food neophobia, (b) average, and (c)
While the existing research has been limited food neophilia. Compared to the latter two
in scope, investigations have centered on a small groups, neophobic children were less likely to
subset of genetic sensitivities to bitter taste, in meet two-thirds of the Recommended Dietary
particular the chemical 6-n-propylthiouracil Allowances (RDAs) and Dietary Reference
(which is also a drug used in the treatment of Intakes (DRIs) of vitamin E. The diets of these
Grave’s disease, which carries an FDA alert children were also characterized by a higher
regarding risk of serious liver damage and poten- intake of saturated fat, less dietary variety, and of
tial life-threatening effects associated with its poorer overall quality, as measured by the USDA
use). Individuals with this specific taste sensitiv- Healthy Eating Index (HEI; 1995). As might be
ity are significantly less likely to try novel foods, expected, neophobic children also consumed
including those commonly accepted among chil- fewer unique foods than their neophilic
dren (such as American cheese and whole milk; counterparts.
Keller et al., 2002). Some have observed a gender In a survey of the eating behaviors of pre-
interaction, in that males consume more fatty school British children, Cooke et al. (2003) dis-
protein products (such as animal-based meat covered that scores on the Child Food Neophobia
products), leading to higher weight-to-height Scale (CFNS; Pliner, 1994) were inversely related
ratios, whereas females demonstrate a more to frequency of parent-reported consumption of
global food avoidance, including fatty meat prod- vegetables, fruit, meat, and eggs. Similar findings
ucts, leading to lower weight-to-height ratios were ascertained by Cooke et al. (2006) in a more
(Keller & Tepper, 2004). detailed analysis of these variables. Consistent
with their earlier study (2003), and in accordance
Dietary Restriction In contrast to the develop- with the findings of Russell and Worsley (2008),
mentally appropriate and adaptive pattern food neophobia was negatively correlated with
described above, a significant minority of chil- consumption of fruit, vegetables, protein foods,
dren and adolescents exhibit such severe levels of and total calories, even after controlling for child
food neophobia that food is restricted to a dys- age, socioeconomic variables, and ethnicity. A
functional degree. Russell and Worsley (2008) comparison of the diets of children with higher
recently investigated the relationships between and lower levels of neophobia yielded nearly
food neophobia and food preferences among a identical results. That is, children with higher
sample of preschoolers recruited from the com- neophobia consumed significantly fewer fruits
munity. The investigators discovered that trait and vegetables, protein foods, and total calories.
food neophobia was negatively related to chil- The relationship between cultural attitudes on
dren’s preferences for all food groups, with sub- food and food neophobia represents an important
stantial correlations between food neophobia and area of future investigation as food neophobic
preferences for vegetables, meats, and fruit. antecedents and consequences may differ by cul-
Significant negative correlations were also ture (Choe & Cho, 2011; Siegrist et al., 2013).
observed between food neophobia and the num-
ber of liked food items, the variety of food prefer- Anorexia Nervosa Picky eating in childhood
ences, and the overall quality of children’s has been demonstrated to increase the risk of
preferences. extreme anorexic symptoms in adolescence. In a
10-year, longitudinal study of over 800 children, significantly decreased (Thomas et al., 2020).
Marchi and Cohen (1990) utilized a logistic Nonetheless, additional investigation into the
regression analysis to identify prospective risks relationship between food neophobia and ARFID
associated with extreme eating disorder symp- is required, particularly empirical investigations
toms. Among other things, they discovered that into the distinctness of the constructs.
(a) pickiness in early and later childhood was a
significant risk factor for extreme symptoms of In summary, studies have just begun to
anorexia in adolescence, and (b) picky eating in uncover the adverse outcomes associated with
later childhood and adolescence was predictive food neophobia. Available research suggests that
of symptoms two years later. A word of caution is food neophobia may unfavorably affect diet and
in order, however. A careful examination of the eating behaviors, including the variety and over-
pickiness construct utilized by Marchi and Cohen all quality of food preferences and consumption.
reveals a construct that is similar, yet clearly dis- This is particularly worrisome, as dietary variety
tinct from food neophobia. Therefore, the extent and diversity are thought to help ensure that an
to which these findings are also true of food neo- adequate assortment of necessary nutrients and
phobia is unclear. other essential dietary components are consumed
(Falciglia et al., 2000; U.S. Department of
Agriculture, 2005). Although less conclusive,
Avoidant/Restrictive Food Intake research has also indicated that picky eating in
Disorder Avoidant/Restrictive Food Intake childhood may increase the risk of developing
Disorder (ARFID) represents a disorder charac- anorexic symptoms in adolescence. It remains to
terized by failing to consume enough nutrients to be seen if food neophobia poses a similar risk and
sufficiently meet one’s biological needs (APA, whether it may lead to ARFID or other eating
2013). To be diagnosed with ARFID, individuals disorders.
must experience significant weight loss or stunted
growth, nutritional deficiency, psychosocial
impairment, or reliance on nutritional supple- Cognitive-Behavioral Approaches
ments or intestinal feeding. As ARFID involves for Food Neophobia
food avoidance or severe food restriction, some
investigators use the terms interchangeably This review thus far illustrates that: (a) food neo-
(APA, 2013) and distinguishing between ARFID phobia is fairly common; (b) general food aver-
and food neophobia can be challenging. Sensory sion is an adaptive response, and reluctance to try
sensitivity has been implicated in both ARFID novel foods is an effort to protect from ingesting
and food neophobia, although lack of interest in harmful substances; (c) alternatively, consump-
food and fear of aversive consequences may be tion of novel foods is also adaptive as it permits
more pronounced with ARFID (Kutbi et al., ingestion of chemicals associated with a healthy
2019; Thomas et al., 2017). Of note, food neo- diverse diet; (d) in extreme forms the avoidance
phobia measures may help differentiate between mechanism prevents consumption of food, even
individuals with ARFID, and individuals with if it comes with dietary risks; and (e) this
anorexia nervosa (Becker et al., 2019) or people proneness to elevated aversive responses to food
with disordered eating (Zickgraf et al., 2016), as may be due, in part, to normal developmental fac-
those with ARFID scored significantly higher on tors, inherited components, and parental
food neophobia. Fortunately, treatment of ARFID behavior.
has demonstrated a similar impact on food neo- These factors imply several possible lines of
phobia. In a study of children and adolescents intervention, depending on the severity of food
receiving cognitive-behavioral therapy for avoidance and willingness to engage in activities
ARFID, 70% of subjects no longer met criteria designed to expand diet choices. In line with
for ARFID posttreatment and food neophobia cognitive-behavioral approaches to therapy, the
most appropriate potential interventions would based on specific parameters (e.g., proximity and
involve exposure, contingency management, or time in contact; see Wolpe, 1992), food hierar-
some combination of these two interventions. In chies may be constructed based on size of food
any case, parent training would also be consid- item, texture, and method of preparation. These
ered crucial for successful treatment. Additionally, are just a few possible dimensions on which food
it is important to note that most people have spe- hierarchies may be developed. An illustration of
cific food likes and dislikes. It is therefore essen- this type of hierarchy is presented in Table 25.1.
tial that clinicians remain sensitive to the goal of Once a food hierarchy is established, the child
expanding the range of accepted foods while also should be provided with daily reinforcement for
maintaining that some food aversions may remain consuming some agreed-upon food listed on the
regardless of efforts to alleviate them. low end of the hierarchy. Once the child becomes
proficient at eating low-level preparations of the
avoided food, the child should be reinforced for
reatment Approach #1: Contingency
T eating preparations that are listed higher on the
Management hierarchy, and so on. Once the hierarchy for a
particular preparation is finished, or close to fin-
For mild food aversion that does not rise to the ished, other foods may be approached to expand
level of impairment (associated with inadequa- the range of foods consumed.
cies in diet), offering contingent rewards for try-
ing new foods can be a viable approach. As noted Table 25.1 Illustrative hierarchy for developing contin-
above, pressure for trying new foods creates neg- gencies to expand food consumption range
ative responses to that class of food (Tuorila & Degree of desirability (0 = not
Mustonen, 2010). Therefore, creating induce- desirable; 10 = highly
ments for trying classes of foods that may fall Texture desirable)
outside the range of acceptable foods, but are Chicken, cooked 0
without skin
near to the core feature that is being avoided, may
Chicken, cooked with 2
be an acceptable means of increasing the range of skin
foods eaten. This essentially combines the notion Chicken, boneless, no 3
of a hierarchy of potentially acceptable foods breading
(ranging from readily acceptable to unquestion- Chicken, boneless, 5
ably rejected) with providing reinforcement for lightly breaded
those food items that would not be readily eaten Chicken, boneless, in 7
strips, breaded
but are low on the hierarchy. For example, if a Chicken nuggets, 9
child accepts only chicken nuggets, he may be small, heavily
persuaded to expand his food choices to breaded breaded
chicken cutlets (a nearby item, but not as small or Method of
as heavily breaded as nuggets). preparation
Chicken, sautéed 1
Setting up the hierarchy may require some ad
Chicken, grilled 3
hoc guesses as to what would constitute accept-
Chicken, grilled with 4
able foods. That is, the clinician may need to light breading
approximate foods that are not exactly matched Chicken, fried with 5
to acceptable foods on a trial-and-error basis to no breading
develop a program of contingency management Chicken, fried, lightly 7
breaded
that will be acceptable to the child and viable for
Chicken, fried, 9
the parent or caregiver to implement. Further, the heavily breaded
features of new foods that are considered “accept- Note: These are for a child who primarily consumes
able” or “unacceptable” can vary based on sev- chicken nuggets but either reluctantly accepts other
eral characteristics. Just as fear hierarchies are chicken preparations or rejects other forms altogether
reatment Approach #2: In Vivo

T that direct exposure to disgust requires more time
and Graduated Exposure to produce habituation (McKay, 2006). It has also
been noted that the conditioning that leads to dis-
For some children, there is a general willingness gust is more resistant to habituation by its very
to try new foods, but a corresponding problem of nature, since it involves evaluative conditioning
lingering aversion that arises when the child has a (de Houwer et al., 2001). That is, when an object
negative gustatory experience. In such instances, is conditioned to elicit a reaction, the accompa-
exposure (in vivo or graduated) may be attempted, nying label attached to it makes it resistant to
but it would constitute small levels of exposure. habituation.
That is, in contrast with in vivo exposure Recent research has suggested that disgust
approaches for feared situations, where massed plays an important role in preparing for the devel-
exposure to feared stimuli is practiced until there opment of aversive stimuli in fear-conditioning
is habituation (for detailed discussion, see experiments. To illustrate, Muris et al. (2008)
Richard & Lauterbach, 2006), it may be more found that when children were informed that spe-
difficult to accomplish true habituation to rejected cific unfamiliar animals were dirty, they were
foods. Indeed, recent analyses have suggested more likely to fear these animals, as compared to
that graduated exposures for food aversion may children who were told these same animals were
help children accept new foods (Dovey et al., clean. Another way in which disgust may operate
2008), but food exposures are unlikely to achieve to increase food avoidance is by observation of
fear habituation. Instead, the role of food expo- the reaction of others to food items. A recent
sures is to expand the range of foods consumed study showed that when adults were presented
and diminish avoidance, but not necessarily to with facial expressions of disgust in conjunction
alter an emotional reaction to different foods. with food items, the willingness to consume the
The hierarchy described in the section related food was decreased, compared to control partici-
to contingency management would serve the pur- pants (Barthomeuf et al., 2009). In light of the
pose of setting the occasion for an exposure- attention bias that individuals with contamination
based approach as well. This can be initiated, fear (Armstrong et al., 2010) and unselected non-
developed, and managed in the office, while also clinical participants (Cisler et al., 2009) show
being implemented at home by parents and care- toward disgust stimuli, it is reasonable to suggest
givers for enhanced generalization. that food neophobia may develop, in large part,
due to a combination of disgust reactions: the
attention bias for minute disgust reactions in oth-
The Special Role of Disgust in Food ers when consuming food as well as the evalua-
Neophobia tive conditioning process that serves as an
etiological mechanism for disgust responses. A
At the beginning, we noted the importance of the preliminary model is illustrated in Fig. 25.1.
omnivore’s dilemma in setting the stage for
understanding food neophobia. This idea also Treatment Considerations Related to Disgust:
suggests that disgust plays a critical role in under- Making Exposure Work In light of the difficulty
standing food aversions and neophobia. Food in producing habituation when there is a strong
neophobia has been positively related to food- disgust reaction, and the proneness to direct
related disgust in both Western and Middle attention to disgust relevant stimuli, applications
Eastern youth (Egolf et al., 2019; Kutbi et al., of both in vivo and graduated exposure proce-
2019). Disgust is covered elsewhere in this book dures require distraction to allow for adequate
(Chap. 20), so we will not dwell on it here. tolerability to the stimuli. This method contrasts
Instead, we will center our discussion on the dif- accepted exposure procedures for fear-based
ficulties posed by exposure with the aim of reduc- stimuli, where distraction is associated with
ing avoidance. Recent analyses have suggested poorer outcome (Hazlett-Stevens & Craske,
Novel food item
Labeling of food
Observation of Attention bias for
other reactions disgust reactions item as
to food in others disgusting
New food item presented
Does it resemble
Ye
No
prior dood item? s
Evaluated for
Rejected as disgust
comparability to
relevant
accepted to foods
Fig. 25.1 Preliminary cognitive-behavioral model for the development of food neophobia
2008). Therefore, we propose applying a set of

appealing distractions while setting up exposure matic substances were identified that Jake found
for foods that have been labeled disgusting by appealing. These included an aromatic candle
children with extensive food avoidance. To illus- and scented shaving cream, as well as a “taste
trate, in a case treated by one of the authors of block” involving a squirt of mouthwash into the
this chapter (DM), a set of strong olfactory dis- mouth immediately prior to tasting new foods
tractions were arranged in advance of trying new (which Jake also deemed acceptable; other pos-
foods. The child presenting for treatment was a sible stimuli include juices or toothpaste). When
9-year-old male with an increasingly limited initiating exposure, the candle was lit, and the
range of acceptable foods due to pronounced dis- shaving cream was wiped just below Jake’s nos-
gust reactions. His food avoidance had become trils in advance of beginning exposure to low
so severe that he was losing weight and had dif- items on the hierarchy. This arrangement is illus-
ficulty finding acceptable foods at school and at trated in Fig. 25.3. Jake responded well to these
summer day camp. He expressed strong hunger activities for low items on the hierarchy, and his
reactions but, at the same time, he was unable to mother was instructed to continue this exercise at
overcome the disgust reaction for a wide range of home. This exercise continued for 15 sessions,
foods. An illustration of the functional arrange- with Jake receiving contingent reinforcement
ment of relevant stimuli for this boy (Jake) is pre- (using a “star chart”) for trying new foods on a
sented in Fig. 25.2. daily basis, as well as contingent rewards for
engaging in treatment on a daily basis with his
mother or father. By the end of treatment, Jake
Following the assessment, a hierarchy of had gained weight and had a body mass index in
potentially acceptable, but presently avoided, the normal range. His gains were maintained at
foods was constructed. In addition, a set of aro-
Intermediary
congition:
“This doesn’t look right,
New Food
It’s yucky”
Item
Food Refusal
Emotional
Reaction (i.e.,
crying)
Disgust Reaction
Disgust reaction
(i.e., gagging)
Fig. 25.2 Functional depiction of food refusal maintenance by disgust in “Jake”
Fig. 25.3 Development Tasting Tray Setup:

Agreed upon items
of exposure procedures “willing to try’.” These were
for novel food items for Preparation in session *cheese
*turkey
“Jake” *ham
Appealing
Aromatic Candles
Target
Scented Shaving
“Tasting Tray”
Cream
Taste block
Taste block: squirt mouth with

mouthwash
three-month follow-up. His progress is illustrated avoidance (such as through pressure on children
in Fig. 25.4. to consume novel or otherwise rejected foods).
Second, some food aversions may be heritable,
such as the aversion associated with specific
Conclusions chemicals present in bitter foods. Third, several
factors associated with disgust appear to play a
The literature relating to cognitive-behavior ther- prominent role in the development and mainte-
apy for food neophobia is extremely limited at nance of food avoidance.
this point. However, basic research on the corre- We have attempted to outline several impor-
lates and causes of food aversion suggests that tant features of food aversion toward developing
several important factors play a role in the prob- a model for treatment. These components include
lem. First, there are several ways that parents and adjusting exposure-based therapy to account for
caregivers, while well-intentioned, worsen food the special limitations in habituation to disgust,
22
21
20
BMI
19
18
17
16
2 3 4 5 6 7 8 9 10 11 12 13 14 15
p
1
u
w-
llo
fo
Sessions
h
t
on
m
e
re
Th
BMI <18.5 considered underweight. Normal weight between 18.5 and 24.5.
• Reached normal range BMI by session 8 and maintained at follow-up.
• BMI calculated by kg/m²
Fig. 25.4 Treatment outcome for “Jake” following cognitive-behavioral therapy for food neophobia
and some potential methods for ensuring success research on food aversions and neophobia within
when attempting either in vivo or graduated a cognitive-behavioral context in order that com-
exposure. While we have been able to demon- prehensive treatment guidelines may be
strate treatment-related improvements by incor- developed.
porating an olfactory or gustatory distraction
while conducting exposure with a severely food
avoidant child, this is by no means to be taken as References
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Anxiety-Related Problems
in Developmental Disabilities 26
Morgan M. McNeel, Emily R. Jellinek,
and Eric A. Storch
Developmental disabilities encompass a range of social skills), and the onset of these impairments
diagnoses that present developmental challenges before the age of 18 years (APA, 2013). Overall,
in language, learning, behavior, and/or physical ID affects approximately 1% of the general popu-
mobility (Zablotsky et al., 2019). While many lation. However, approximately 33% of individu-
conditions are included in this group (e.g., als with ASD are also diagnosed with ID. The
ADHD, learning disability), this chapter will prevalence of ID does not differ by race and eth-
focus exclusively on anxiety in the context of nicity, yet it is more likely to be diagnosed in
autism spectrum disorder (ASD) and intellectual males than females (Maenner et al., 2020; Maulik
disability (ID). et al., 2013).
Autism spectrum disorder is characterized by Anxiety disorders commonly co-occur with
impairments in social interactions and communi- developmental disabilities. Prevalence estimates
cation and the presence of restricted, repetitive suggest that 7–34% of children with ID have
behaviors (American Psychiatric Association, comorbid anxiety disorders (Buckley et al.,
2013). The prevalence of ASD is approximately 2020). The lifetime prevalence for anxiety disor-
1 in 54 children (Maenner et al., 2020); males are ders among individuals with ASD is 42%, with
4.3 times more likely to be diagnosed than approximately 40% of children with ASD having
females (Maenner et al., 2020). Despite dispari- at least one anxiety disorder (Hollocks et al.,
ties in diagnosis and early intervention among 2019; Van Steensel et al., 2011). The most com-
Black and Hispanic children, ASD is similarly mon comorbid anxiety disorders among children
prevalent across all races, ethnicities, and socio- with ASD are specific phobias (30–44%), social
economic status (SES) groups (Durkin et al., anxiety disorder (SAD; 17–30%), generalized
2017). anxiety disorder (GAD; 15–35%), separation
Intellectual disability, which was formerly anxiety (9–38%), and obsessive-compulsive dis-
referred to as “mental retardation,” is marked by order (OCD; 17–30%) (Van Steensel et al., 2011;
the presence of significant impairment in intel- White et al., 2009).
lectual functioning indicated by an intelligence Children with ASD and comorbid anxiety dis-
quotient (IQ) below or equal to 70, adaptive orders are more likely to experience increased
behavior deficits (e.g., caring for self, autonomy, impairment compared to youth with ASD with-
out anxiety, as anxiety can exacerbate ASD-
M. M. McNeel · E. R. Jellinek · E. A. Storch (*) related symptoms (White et al., 2009). The
Department of Psychiatry and Behavioral Sciences, presence of anxiety and ASD may contribute to
Baylor College of Medicine, Houston, TX, USA greater social difficulties, emotion regulation
e-mail: Eric.Storch@bcm.edu
https://doi.org/10.1007/978-3-031-14080-8_26
380 M. M. McNeel et al.
challenges, and the presence of disruptive and developmental disabilities, for example, are more
noncompliant behaviors (Kerns et al., 2016a; likely to express anxiety or fear through problem
Wood & Gadow, 2010). These challenges are behavior, such as aggression, self-injury, and tan-
indicative of the need for accurate and effective trums (White et al., 2009). These behaviors are
assessment and intervention approaches that will often used to avoid or escape situations or tasks
aid in mitigating the associated impairment expe- and present alongside emotional distress, but it
rienced by youth with ASD and/or ID and can be difficult to determine if anxiety is part of
anxiety. the function of the behavior. Understanding the
function of avoidance behaviors is important for
both the accurate assessment of anxiety as well as
Considerations for Anxiety appropriate goal selection and treatment plan-
and Developmental Disabilities ning. Developmental differences have also been
found to impact the content of anxiety. For exam-
Given heterogeneity in intellectual functioning, ple, for individuals with ID, fears that may be
communication skills, and behavior, there are a developmentally appropriate at a younger age
number of special considerations when assessing may persist into adolescence and adulthood
and treating anxiety among individuals with ASD (Gullone, 1996). Further, individuals with ASD
and/or ID. For example, impairments in commu- may present with fears of an unusual focus (Kerns
nication and social skills, which are common et al., 2014). More specifically, for example, fears
among individuals with ASD and/or ID (APA, that may be related to atypical sensory experi-
2013), may limit the child’s ability to report their ences are common (e.g., fear of loud sounds,
thoughts, affective states, and psychological sen- beards, automatic toilets, mechanical objects;
sations. Communication impairments inherent to Kerns et al., 2014).
ASD and ID are perhaps the most salient chal- These aforementioned considerations present
lenge, as they impact not only the individual’s challenges for both the assessment and treatment
ability to communicate their thoughts and feel- of anxiety among individuals with developmental
ings but also the caregivers’ knowledge of their disabilities. Thus, the remainder of this chapter
thoughts and feelings. This impacts the utility of will discuss existing research and clinical impli-
both self- and other-informant reports, and thus, a cations/suggestions regarding accurate identifi-
multimodal approach is advocated. cation of and effective treatment of anxiety when
It is also important to note shared features of working with this population.
anxiety and developmental disabilities, which
can also complicate the assessment and treatment
process among this population. For example, Assessment of Anxiety
core symptoms of ASD include restricted, repeti- in Developmental Disabilities
tive interests and behaviors, which may be diffi-
cult to differentiate from rituals in Reliable assessment of anxiety is important to
obsessive-compulsive disorder (OCD). accurately classify symptoms and inform treat-
Additionally, avoidance of certain situations ment planning. Given the aforementioned chal-
(e.g., social interactions) is common in ASD, but lenges associated with assessing anxiety among
may also be indicative of certain anxiety disor- individuals with developmental disabilities, a
ders. Determining if such symptoms should be multimodal, multi-informant assessment process
conceptualized as part of ASD or as a separate that is methodical and empirically grounded is
comorbid anxiety disorder presents a challenge essential. Assessment methods should include
for clinicians (White et al., 2009). the use of interviews, questionnaires and rating
Another challenge is that symptoms of anxi- scales, and direct observations.
ety may present differently in individuals with
developmental disabilities. Individuals with
26 Anxiety-Related Problems in Developmental Disabilities 381
Clinical Interviews symptoms of ASD and symptoms of other diag-

noses, including anxiety. While this approach
Clinical interviews, though more time consuming may make it more stringent than other interviews
than other methods, allow for more detailed that do not differentiate (Mazefsky et al., 2012),
information gathering based on both verbal OCD was the only anxiety disorder examined
reports and direct observations during the assess- psychometrically. Compared to the ADIS, it is
ment. Most of the semi-structured clinical inter- not as comprehensive and it still takes 1–3 h to
views used to assess anxiety in youth with complete, but it required less training to adminis-
developmental disabilities were initially designed ter and is a free measure.
for use with typically developing youth. However, Structured clinical interviews have also been
two measures have been modified specifically for used to assess comorbid psychiatric disorders,
use with ASD. including anxiety, in youth with developmental
The Anxiety Disorders Interview Schedule for disabilities. Of them, the Children’s Interview for
DSM-IV, Child and Parent Versions (ADIS-IV-- Psychiatric Symptoms – Parent Version (P-ChIPS;
C/P) (Silverman & Albano, 1996) are semi- ages 6–17) (Fristad et al., 1998) is the only one
structured interviews to assess anxiety and related that has reported reliability and validity in ASD.
disorders in children ages 7–18 years. It is con- It is considerably shorter to administer than the
sidered the “gold-standard” for assessing anxiety aforementioned semi-structured interviews.
in typically developing youth and has the most Unlike other interviews, the P-ChIPS has also
research support for assessing anxiety in youth been examined in research studies with youth
with ASD and IQs > 70. The ADIS-C/P has dem- with IQs ranging from 42 to 150 (Witwer et al.,
onstrated inter-rater reliability (0.77–1.00; Ung 2012). In youth with IQs < 70, the P-ChIPS has
et al., 2014), sensitivity to change (White et al., demonstrated inter-rater reliability for phobias,
2012; Wood et al., 2009), and convergent and generalized, separation, and social anxiety disor-
divergent validity in youth with ASD seeking ders, but more limited inter-rater agreement for
anxiety treatment (Renno & Wood, 2013). It OCD symptoms (Witwer et al., 2012).
should also be noted that some studies have found
poor agreement between child and parent (Storch
et al., 2012). Another limitation is the administra- Questionnaires and Rating Scales
tion time, which can be up to 2 h. The Autism
Spectrum Addendum to ADIS-P (ADIS/ASA) Self-Report Questionnaires
(Kerns et al., 2017) was later developed as a sup- While self-report questionnaires are the most
plement to the ADIS-IV-C/P. It includes a set of commonly used formal measures for assessing
guidelines designed to differentiate traditional anxiety in both individuals with and without
DSM anxiety disorders in ASD from ambiguous developmental disabilities, few of these instru-
symptoms often present in ASD (e.g., worries ments are specifically designed to assess anxiety
regarding routine or changes in the environment) in developmental disabilities. Among them, the
and has been found to have strong psychometric Multidimensional Anxiety Scale for Children
properties when used with the ADIS. A fifth edi- (MASC-C) (March et al., 1997), the Screen for
tion of the ADIS is reportedly forthcoming. Child Anxiety-Related Emotional Disorders
The Autism Comorbidity Interview – Present (SCARED-C) (Birmaher et al., 1997), and the
and Lifetime Version (ACI-PL) (Leyfer et al., Spence Children’s Anxiety Scale (SCAS) (Spence,
2006) is another semi-structured diagnostic inter- 1998) are the most well-researched. However,
view that can be used for youth with ASD. It is a findings regarding psychometrics are inconsis-
modified version of the Kiddie Schedule for tent and many studies have reported poor
Affective Disorders and Schizophrenia (K-SADS; child/parent agreement. Given this, and the mea-
ages 5–17) (Kaufman et al., 1997). The ACI-PL sures’ clear emphasis on language, they may not
was created to differentiate between the core be appropriate for all individuals with ASD and/
or ID (Lecavalier et al., 2014). The Revised Child dence for convergent validity (Henderson et al.,
Anxiety and Depression Scale (RCADS) 2006).
(Chorpita et al., 2000), however, may be a more Most of the aforementioned measures share
suitable self-report measure for this population, the limitations of primarily only being examined
as previous investigations have found it to be use- in youth with individuals who have average or
ful for individuals with ID (e.g., Kaat & above average IQ and/or greater verbal abilities.
Lecavalier, 2015). An adapted version of the While there are known challenges to developing
RCADS, the Anxiety Scale for Children with sound measures for individuals with ID given
ASD, Parent and Child versions (ASC-ASD) limitations associated with communication, cog-
(Rodgers et al., 2016), includes additional items nition, and comprehension, some evidence sup-
related to sensory anxiety, intolerance of uncer- ports the feasibility of reliable and valid modified
tainty, and phobias, and it shows promising psy- self-reports for individuals with ID (Hagopian &
chometric properties for youth with fluent speech. Jennett, 2008). Two specific measures, the Fear
The Revised Children’s Manifest Anxiety Survey Schedule for Children – Revised
Scale (RCMAS) (Reynolds & Richmond, 1978) is (FSSC-R) and the Fear Survey for Children with
a self-report questionnaire that may be useful as a and without Mental Retardation (FSCMR), were
screening measure of anxiety for youth with developed with specific modifications for this
developmental disabilities. It consists of 37 yes/ population: verbal and visual presentation, sim-
no questions across three anxiety domains (phys- plified language, and neutral items to assess
iological, worry/oversensitivity, and social con- acquiescence or choosing the more positive
cerns/concentration), measuring the presence of response (Hagopian & Jennett, 2008). Both the
symptoms based on child self-report rather than FSSC-R and the FSCMR have been psychometri-
the severity. Despite good internal consistency cally evaluated with youth with ID (Reardon
and some evidence for specificity and sensitivity et al., 2015).
(Mazefsky et al., 2011) and a second edition
(RCMAS-2), which has demonstrated improved ther-Informant Rating Scales
O
psychometric properties, updated norms, and Other informants can also complete question-
broader item content coverage, it is not an appro- naires to provide additional information. This is
priate outcome measure for these reasons especially helpful when assessing youth with
(Lecavalier et al., 2014). developmental disabilities, given the aforemen-
The reliability and validity of the State-Trait tioned challenges and limitations of self-report
Anxiety Inventory for Children (STAIC) measures with this population. The MASC and
(Speilberger, 1973) has not been evaluated in MASC-2, SCARED, RCADS, SCAS, and SWQ
developmental disabilities, but it may be useful all have versions for other informants to com-
for distinguishing trait and state anxiety in ASD plete. Agreement between child and parent-report
(Lanni et al., 2012). Further, a number of self- varies across these measures but has been found
reports designed for typically developing chil- to be weaker for the SWQ and MASC.
dren to assess social anxiety (e.g., Social Anxiety Another other-informant-report measure is the
Scale for Children – Revised [SASC-R], Social 20-item version the Child and Adolescent
Anxiety Scale for Adolescents [SAS-A], Social Symptom Inventory – 4th Edition Revised
Worries Questionnaire [SWQ]) may also have (CASI-4R) (Gadow & Sprafkin, 2002), which
utility in ASD. While the SWQ is relatively was created to assess anxiety, specifically in indi-
under-researched with few psychometric data viduals with ASD (Sukhodolsky et al., 2008).
(Kerns et al., 2016b), investigations using the Notably, most of the people included in the mea-
SASC-R/SAS-S have demonstrated treatment surement study had ID (Sukhodolsky et al.,
sensitivity (Kaboski et al., 2015), good internal 2008). Findings demonstrated good internal con-
consistency (Kaboski et al., 2015), and some evi- sistency across children with and without
c ognitive impairment and support its use as an properties of the anxiety subscales in these mea-
outcome measure (Sukhodolsky et al., 2008). sures with individuals with disabilities. In the
The Parent-Rated Anxiety Scale for ASD meantime, they may be helpful as a screening
(PRAS-ASD) (Scahill et al., 2019) is the newest measure, but should be followed by a more com-
parent-report measure for anxiety in children prehensive assessment including interviews and
with ASD, which it was specifically designed to direct behavioral observation.
assess. The 25-item scale demonstrated discrimi-
nant validity, excellent internal consistency, item
response theory (IRT) reliability, and test–retest Clinician-Rated Symptom Measures
reliability (Scahill et al., 2019).
The Autism Spectrum Disorder – Comorbid The Pediatric Anxiety Rating Scale (PARS;
for Children (ASD-CC) (Matson et al., 2009). is RUPP, 2002) was designed as a treatment out-
an additional measure indented for other infor- come measure and provides a continuous mea-
mants to complete. It is a 49-item scale with sure of anxiety symptoms in youth ages
established reliability and construct validity used 6–17 years based on child and parent reports and
to measure comorbid psychopathology in chil- clinical judgment. While the measure appears
dren with ASD and varying intellectual function- sensitive to change in children with ASD and
ing. When assessing anxiety within the context of IQs > 70 (Storch et al., 2012), its psychometric
ASD, the Worry/Depressed and Avoidant sub- properties with this population are variable.
scales are the most helpful (Rieske et al., 2013). Storch et al. (2012) found excellent test–retest
While the Worried/Depressed subscale has dem- reliability and inter-rater reliability; however,
onstrated convergent and divergent validity there was also low internal consistency and con-
(Rieske et al., 2013) and moderately good inter- vergent and divergent validity were only partially
nal consistency (Davis et al., 2011), more supported. Despite promising findings, it should
research is needed to thoroughly investigate also be noted that given the reliance on fluent lan-
retest reliability, sensitivity, and specificity. guage for the child interview, the use of the PARS
While it has not been tested with individuals may be limited to those who are more verbal and/
with ASD, the Anxiety, Depression, and Mood or have a higher IQ (Lecavalier et al., 2014).
Scale (ADAMS) (Esbensen et al., 2003) is an More research is needed to improve the sensitiv-
informant-rated measure that has shown promis- ity of the PARS, particularly in lower-risk sam-
ing psychometrics in with individuals with ID – ples, as well as to investigate its utility for
especially for screening for OCD. It is a brief, assessing anxiety among individuals with
28-item scale of behaviorally based mood and IQs < 70.
anxiety symptoms. Additional other-informant Clinician-rated scales such as the Children’s
measures that may be appropriate to use across Yale-Brown Obsessive-Compulsive Scale
varying intellectual functioning include the Modified for Pervasive Developmental Disorders
Developmental Behavior Checklist (DBC) (CY-BOCS PDD) (Scahill et al., 2006) and the
(Brereton et al., 2006), the Nisonger Child CY-BOCS for Children with Autism Spectrum
Behavior Rating Form (NCBRF) (Aman et al., Disorder (CY-BOCS ASD) (Scahill et al., 2014)
1996), and the Baby and Infant Screen for have also been developed to measure the severity
Children with aUtIsm Traits (BISCUIT) – Part II of repetitive behaviors in children (ages 5–17)
(Matson et al., 2009). While these scales are who have ASD or other developmental disabili-
designed to assess a broad range of behaviors, ties. These represent modifications of the
they all include anxiety subscales and have been Children’s Yale-Brown Obsessive-Compulsive
used in some studies to assess anxiety problems Scale – First and Second Editions (CY-BOCS;
in youth with ASD and ID (e.g., Bakken et al., Scahill et al., 1997; Storch et al., 2019), which
2010; Bradley et al., 2004). More research is are often considered the “gold standard” measures
needed to further investigate the psychometric for assessment of child OCD symptoms. The
CY-BOCS PDD is a semi-structured interview involves assessing the child’s avoidance response,
administered to the child’s parent (Scahill et al., subjective level of anxiety, physiological reac-
2006). The CY-BOCS ASD includes a 23-item tions, and/or behavioral responses while progres-
symptom checklist and five severity scales: Time sively exposing them to the feared stimulus
Spent, Interference, Distress, Resistance, and (Hagopian & Jennett, 2008). In addition to dur-
Control. It also includes a five-component system ing the initial assessment, the BAT can also be
for classifying repetitive behaviors in ASD used during and after treatment to evaluate
(hoarding and ritualistic behavior, sensory and outcomes.
arranging behavior, sameness and self-injurious For children with more generalized anxiety,
behavior, stereotypy, restricted interests) (Scahill when it is challenging to identify or control
et al., 2014). Both measures have established reli- anxiety-provoking stimuli, it may not be feasible
ability and convergent validity and are sensitive to conduct a BAT (Hagopian & Jennett, 2008). In
to change (Scahill et al., 2006). Despite strong these cases, naturalistic observations during the
psychometric properties, it should also be noted other portions of the assessment and/or in the
that these measures were developed to assess the child’s other environments (e.g., home, school,
severity of repetitive behaviors, and given the community) can be used to further assess anxiety.
measure’s reliance on compulsions (without Enlisting care providers to conduct behavioral
assessing obsessions), it can be difficult to accu- monitoring (i.e., observe- and record-specific
rately determine the presence of OCD. Thus, the behaviors) in the child’s natural setting(s) can be
original CY-BOCS, ACI, and ADIS/ASA may be especially effective. This approach can also be
more useful when differential diagnosis of ASD used for evaluating treatment response.
and OCD is required.
Assessment of Skills
Direct Observation As noted previously, there are many challenges
Direct behavioral observations are often needed associated with the assessment of anxiety among
to clarify and validate findings and hypotheses in individuals with developmental disabilities. As
gathered from interviews and questionnaires such, when determining the appropriate attribu-
regarding the controlling variables of anxiety. tion of symptoms (i.e., to either ASD/ID or anxi-
This is especially the case for youth with devel- ety) and developing a treatment plan, it is often
opmental disabilities, given the aforementioned important to gather additional data about the indi-
challenges with self- and other-informant reports vidual’s skills and deficits. Skill areas that should
(Hagopian & Jennett, 2008). For individuals with be considered when assessing and treating anxi-
comorbid ID and/or minimal verbal abilities, ety in individuals with developmental disabilities
anxiety must often be inferred from their overt include social skills, communication deficits, lei-
behavior or “fear responses” through direct sure skill deficits, presence of restricted and ste-
observation (Rosen et al., 2016). Direct observa- reotyped patterns of behavior, stimulus
tion allows for more detailed and possibly more over-selectivity, and deficits in varying behavior
accurate information about the behaviors an indi- across different contexts.
vidual displays when they are anxious as well as
the antecedents and consequences related to their
anxiety. Treatment of Anxiety
When presentation of the avoided stimulus in in Developmental Disabilities
a controlled manner is possible, the Behavioral
Avoidance Test (BAT) can be employed Given the prevalence of comorbid anxiety among
(Ollendick et al., 2013). This is often the case individuals with developmental disabilities, as
with anxiety that is elicited by a specific stimulus well as the associated impairment of the comor-
or classes of stimuli (e.g., social phobia, specific bid diagnoses, a body of research on effective
phobia, or separation anxiety disorder). The BAT treatments has emerged. While psychosocial
interventions used to treat anxiety among typi- special interests, and providing teaching and
cally developing individuals may also be effec- communication strategies in session (e.g., social
tive among individuals with developmental skills and longer sessions) as modifications to
disabilities (see Nadeau et al., 2011; Sukhodolsky graduated exposures that beneficial for children
et al., 2013), this unique and heterogeneous pop- with developmental disabilities (Wood et al.,
ulation warrants special considerations when 2020).
applying traditional treatment approaches such as
exposure therapy and cognitive-behavioral ther- Cognitive-Behavioral Treatment
apy. More research is needed to further investi- Approaches
gate the efficacy of various psychosocial Cognitive-behavioral therapy (CBT) is a long-
interventions for anxiety among individuals with standing treatment that has robust empirical sup-
developmental disabilities, but the existing port for use with youth with anxiety (Banneyer
research base provides promising results regard- et al., 2018; Wang et al., 2017). More recently,
ing the use of adapted behavioral and cognitive- research has supported the use of adapted
behavioral approaches. cognitive-behavioral treatment approaches for
children with developmental disabilities (Hronis
et al., 2019; Hunsche & Kerns, 2019). Adaptions
Intervention Studies to researched CBT protocols included
caregiver/family inclusion for most treatment
Behavioral Treatment/Exposure sessions, parent-delivered contingent reward sys-
Therapy Approaches tems, revised cognitive therapy modules, and
Graduated exposures, otherwise known as expo- modules that were implemented as needed (social
sure therapy (ET) or exposure and response pre- and adaptive skills deficits, social and school
vention (ERP), is a well-established treatment for issues, rewards/consequences, incorporation of
anxiety disorders in typically developing children special interests, and disruptive behavior man-
(Whiteside et al., 2020). The goal of graduated agement) (Storch et al., 2015b). Exposure ther-
exposures is to decrease the negative reinforce- apy remains a cornerstone of these interventions
ment associated with avoidance of anxiety- and is discussed previously.
provoking stimuli by promoting habituation to Research has demonstrated the effectiveness
the feared stimuli. Through gradually and repeat- of adapted CBT protocols among children with
edly exposing child to a feared stimulus, the trig- ASD and anxiety (Reaven et al., 2012; Storch
ger should elicit less anxiety and et al., 2013; Wood et al., 2009, 2015). Randomized
anxiety-minimizing behaviors (e.g., avoidance, control trials of an adapted exposure-based CBT
compulsions) are minimized (Craske et al., protocol, Behavioral Interventions for Anxiety in
2014). Children with Autism (BIACA), found the treat-
For children with developmental disabilities, ment to be treatment-as-usual (TAU) effective
who may have intellectual deficits, executive compared to treatment as usual for children ages
functioning difficulties, or exhibit symptoms of 11–16, and superior to TAU and coping cat for
cognitive rigidity and social skills deficits, gradu- children ages 7–11 for children with ASD and
ated exposures have been found to be effective in anxiety (Storch et al., 2015a, b; Wood et al.,
addressing anxiety symptoms in this population, 2020). It is important to note that many studies
despite these challenges (Ryan et al., 2017). have investigated the use of such protocols with
Modifications should be made to typical gradu- children with ASD and there are few studies that
ated exposure protocols to address the unique have investigated the used of adapted CBT treat-
needs of children with developmental disabilities ments for use with adolescents with ASD and
and anxiety. Recent research has highlighted the anxiety disorders (Storch et al., 2015a, b; White
effectiveness of involving caregivers in graduated et al., 2013; Wood et al., 2015). Group CBT
exposures, using reward contingencies that target approaches have been d eveloped and investigated
for both children and adolescents with ASD and given the dual diagnoses. Goals should focus on
anxiety. Several randomized controlled trials improving the individual’s quality of life instead
have demonstrated improvements in anxiety of or in addition to adhering to social norms, and
symptoms following the use of these interven- treatment goals should be socially and culturally
tions (Chalfant et al., 2007; McConachie et al., valid to the individual and family. The remainder
2014; Reaven et al., 2012; Sofronoff et al., 2005; of this section will discuss additional anxiety
Sung et al., 2011). treatment considerations for youth with develop-
There is limited research investigated the use mental disabilities.
of cognitive-behavioral treatment approaches for
children with ID and anxiety. Aspects of Communication and Teaching
cognitive-behavioral treatment approaches such Strategies
as psychoeducation, cognitive reappraisal, and For some individuals with anxiety and ASD and/
ERP practices with reinforcement have been or ID, social communication and behavioral chal-
shown to be effective in anxiety reduction for lenges may warrant additional treatment compo-
children with ASD and ID (Moskowitz et al., nents to facilitate engagement and ensure
2017). Further, Hronis et al. (2019) examined the progress with behavioral or cognitive-behavioral
use of Fearless Me!, an online and group CBT interventions. Various teaching strategies such as
program, for 21 adolescents with moderate and prompting and modeling, while not always con-
mild ID and anxiety. Their findings suggested sidered a primary component of the traditional
that their treatment significantly reduced anxiety, treatment protocol, can be helpful additions when
providing preliminary evidence for the use of an working with this population. For example, these
adapted CBT program for adolescents with ID approaches may facilitate the individual’s under-
(Hronis et al., 2019). Additional modifications to standing of how to execute an exposure correctly
CBT approaches such as including multiple and the reinforcement contingencies in place.
modalities of treatment (e.g., online and face to When integrating these strategies with exposure-
face), frequent sessions, the use of concrete based approaches, it may be helpful to begin
examples, behavioral intervention plans, and pos- teaching the process through a simulation using a
itive behavior supports may be needed to address neutral stimulus instead of a feared one to
the unique needs of children and adolescents increase the likelihood of successful completion
with ID (Hronis et al., 2019; Moskowitz et al., and thus allow for learning. For individuals who
2017). are unable to understand verbal instructions,
these learning trials may need to be repeated
prior to initiating graduated exposure to feared
Considerations for Anxiety Treatment stimuli. Flexibly using different variations of
in Developmental Disabilities teaching strategies, such as prompting and mod-
eling, is advantageous regardless of developmen-
Given the core symptoms of ASD and ID, as well tal and verbal level.
as the heterogeneity of developmental disabili- Modeling involves demonstrating what the
ties, special considerations are warranted when individual is supposed to do, with the intent of
applying standard anxiety treatment approaches them learning through observation and imitating
to this population. It is important to ensure the the behavior. This can be useful to integrate when
materials and presentation are developmentally teaching the individual new skills within the con-
appropriate. This may involve, for example, more text of anxiety treatment (e.g., coping skills,
concrete and visual strategies, simplified lan- exposure tasks, social skills). Children with
guage, slower pace, more caregiver involvement, developmental disabilities may not be inclined to
or more emphasis on the behavioral components observe and imitate the model, so supplementing
of treatment. With this population, it is also the demonstration with other visualizations such
essential to consider the appropriateness of goals as pictures or videos may also be helpful.
Verbal, visual, and physical prompts can also Behavioral Strategies

be an effective way to facilitate a child’s skill
development, including within the context of Contingent Reinforcement
anxiety treatment. The level of prompting should Practice is an important component of anxiety
directly reflect the amount of assistance required intervention – both for cognitive strategies and
for the child to complete the skill. As such, they exposure to feared stimuli. However, it can be
should be lessened over time as the individual especially challenging to motivate children with
learns the process. The type (or types) of prompts ASD and/or ID to engage in non-preferred activi-
used will be determined by what is being taught ties. ASD has also been conceptualized as having
as well as the child’s developmental level and diminished social motivation (Chevallier et al.,
current skill level. For example, when working 2012). Thus, the intrinsic and social motivation
with individuals who understand verbal prompts that may be sufficient for a typically developing
and are able to independently complete the task, child to fully engage in anxiety treatment may
verbal prompts and cues may be sufficient. Visual not be enough for a child with a developmental
prompts such as gestures or pictures can be help- disability. As such, it is important to consider
ful when working with children who are not able ways to increase an individual’s motivation to
to understand verbal prompts. When working engage in practice (Abramowitz, 2013). One
with an individual who does not understand versuch method for increasing motivation is contin-
bal prompts and also is not familiar with the skill, gent reinforcement, which involves providing
physical prompts (e.g., hand-over-hand guid- rewards for engaging in specific tasks (e.g., expo-
ance) may be necessary to help them practice the sures) or exhibiting certain behaviors (e.g., cop-
movement required. ing skills). The result is increased motivation to
Teaching and practicing social skills or social repeat the task or behavior, which is essential to
communication strategies may be beneficial to facilitate the learning process.
integrate into exposure practice, as youth with There are several important considerations
ASD and/or ID have social and adaptive skills regarding the integration of contingent reinforce-
challenges (Klin et al., 2007). Anxiety, which can ment within the context of anxiety treatment.
be described as a “won’t do” reaction to situa- First, it is important to consider what the reward
tions, where there are unrealistic fears and per- will be. Types of rewards include tangible or
ceptions of inadequacy that create barriers to physical/material rewards (e.g., toys, money) and
situations, is further compounded by social and intangible or nonmaterial rewards (e.g., praise,
adaptive skills deficits. These challenges result in time doing a preferred activity) (Kazdin, 2013). It
a “can’t do” response, rendering actual barriers to is essential that the reward is meaningful to the
the youth’s ability to navigate anxiety-provoking child and that they are interested in and motivated
situations in addition to the unrealistic fears and by it. Because of this, clinicians should work
perceptions of anxiety the child is experiencing with the individual and family to choose rewards
(Wood et al., 2009). Thus, to effectively treat based on their preferences (Lee et al., 2010).
anxiety, it is important to assess for skill deficits Systematic preference assessments can be help-
that may compound anxiety and then integrate ful in identifying preferred items and rewards
teaching strategies into treatment to build social (Hagopian et al., 2004). They may consist of
and adaptive skills. Incorporating direct teaching interviewing caregivers and/or the individual
and modeling into treatment and integrating these directly about their preferences, observing the
skills with exposures can increase the effective- individual identify preferences within a free-
ness of exposure-based CBT for children with choice context (e.g., selecting rewards from a list
ASD and/or ID (Wood et al., 2015). of options), or utilizing structured preference
assessments (Karsten et al., 2011). Preferred
rewards are particularly effective when working
with individuals with ASD, as this population
often develops restricted interests (Danial & mation regarding functional relationships
Wood, 2013). Using conversations, activities, or between the child’s anxious behaviors and how
tangible items related to an individual’s special family members may be reinforcing and main-
interest as rewards is a strategic way to integrate taining the anxiety. Continued family involve-
special interests. ment then allows the clinician to address family
The success of contingent reinforcement is accommodation in addition to the child’s anxiety
also dependent on correct implementation. When directly through intervention, which is likely to
using this strategy, it is important to deliver the cause greater and more lasting progress.
reward as soon as possible after the child com- For individuals with developmental disabili-
pletes the desired behavior (e.g., practicing a ties who are often supported by caregivers, their
coping skill or completing an exposure) (Piazza involvement is even more essential. In fact, how
et al., 2011). This strengthens the child’s associa- much a caregiver is involved in treatment can be
tion between the behavior and the reward, mak- based on the level of support the child needs from
ing them more likely to engage in the behavior them. When the caregiver plays a large role in the
again in the future. It is also important that the individual’s daily life, he/she is an integral part of
reward is exclusively contingent on attempting anxiety treatment by learning how to respond to
the desired behavior. In other words, it should not the patient’s anxiety, providing additional infor-
be accessible freely or through other means. A mation and support during sessions, and leading
child is less likely to engage in a challenging task skills and exposure practice at home. The level of
to earn, for example, time on his/her tablet, if he/ family involvement will depend on a number of
she know he/she will get to play on his/her tablet factors, including the child’s developmental level
after dinner anyways. Finally, it is also important and other individual and family factors.
to vary rewards. The strength of the reward During treatment, family members and care-
should reflect how challenging the desired behav- givers should receive psychoeducation on accom-
ior is for the child. Sometimes it is important to modation and how to appropriately respond to
change rewards to reflect an individual’s new anxious behaviors. They should then receive sup-
interest. Varying rewards is essential to maintain port in identifying their own accommodating
their value and effectiveness (Wine & Wilder, behaviors and replacing them with relevant
2009). behavior management principles. It is also impor-
tant to normalize the accommodation of anxious
aregiver and Family Involvement
C behaviors and not place blame on the family in
Caregiver and family involvement is essential order to maintain a positive therapeutic alliance.
when working with children and adolescents, as
family systems often contribute to the mainte-
nance and persistence of anxious behaviors Conclusion
(Abramowitz et al., 2019; Ginsburg et al., 2004).
Family members often accommodate anxious Anxiety disorders commonly occur with devel-
behaviors by allowing avoidance of feared situa- opmental disabilities. Children with ASD and/or
tions, permitting escape from anxious situations, ID and a comorbid anxiety disorder are more
assuming responsibilities, and providing reassur- likely to experience increased impairment com-
ance. While they do so in an attempt to reduce the pared to those without anxiety. The heterogeneity
child’s anxiety, these accommodations ultimately in intellectual functioning, communication skills,
hinder treatment if not addressed (Storch et al., and behavior among individuals with develop-
2008). This is seen across typically developing mental disabilities contribute to a number of
children with anxiety and those with develop- challenges when assessing and treating anxiety in
mental disabilities (Frank et al., 2020; Storch this population. Despite challenges associated
et al., 2015a, b). When the family is involved in with assessing and treating anxiety in this hetero-
treatment, the clinician is able to gain more infor- geneous population, accurate and effective
e valuation and intervention methods are vital for Institute of Child Health & Human Development of the
National Institutes of Health under Award Number
supporting and promoting positive outcomes for P50HD103555 for use of the Clinical Translational and
these individuals and their families. Preclinical and Clinical Core facilities. The content is
A methodical and empirically grounded mul- solely the responsibility of the authors and does not neces-
timodal, multi-informant assessment process is sarily represent the official views of the National Institutes
of Health.
essential when identifying and conceptualizing
comorbid anxiety in individuals with ASD and/or
ID. Assessment methods should include the use
of interviews, questionnaires and rating scales,
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Treatment of Youth Anxiety
in the Context of Family 27
Dysfunction and Accommodation
Rebecca G. Etkin and Eli R. Lebowitz
Introduction that stand out for their focus on improving family

functioning and/or reducing accommodation as a
Family dysfunction refers to a range of difficul- means to child and adolescent recovery. We con-
ties or disruptions within the family system that clude with a discussion of future directions for
negatively impact child and adolescent develop- research on the treatment of child and adolescent
ment and well-being. While family dysfunction anxiety and OCD in severely dysfunctional fami-
is associated with child and adolescent psychopa- lies. Henceforth and throughout, we refer to chil-
thology more broadly, it also has clear links to dren and adolescents as “youth” and to anxiety
anxiety disorders and obsessive-compulsive dis- disorders and OCD as “anxiety,” unless other-
order (OCD). In the sections below, we take a wise specified (i.e., if referring to a specific
closer look at the different ways in which fami- developmental period or disorder).
lies may experience dysfunction, and how severe
dysfunction may both stem from and contribute
to child and adolescent anxiety and OCD. We n Overview of Family Dysfunction
A
specifically highlight family accommodation in and Youth Anxiety
our discussion, as it represents a highly prevalent
behavior within families of anxious children and Family dysfunction is a broad term that encapsu-
adolescents that is entwined with dysfunction lates a range of family processes, dynamics, and
and has relevance to the maintenance and treat- behaviors that are detrimental to the well-being of
ment of anxiety. its members. Family systems theory posits that
Following this overview, we turn our focus to dysfunction can be traced to problems with the
the treatment of child and adolescent anxiety and boundaries delineating different family subsys-
OCD in the context of severe family dysfunction tems (e.g., parent–child relationships, the marital
and accommodation. While numerous approaches relationship) (Minuchin, 1974). Clear and appro-
to treating child and adolescent anxiety and OCD priate boundaries promote positive functioning
incorporate families, few of these target family within the family (e.g., effective communication,
dysfunction as the key mechanism of change. We appropriate warmth and power), which in turn fos-
review the evidence-based treatment approaches ters positive youth outcomes. Conversely, bound-
aries that are overly rigid or overly diffuse may
R. G. Etkin · E. R. Lebowitz (*) result in dysfunction (e.g., conflict, disengage-
Child Study Center, Yale School of Medicine, New
Haven, CT, USA ment, enmeshment) that negatively impacts youth
e-mail: eli.lebowitz@yale.edu development (Minuchin, 1974; Olson, 2000).
https://doi.org/10.1007/978-3-031-14080-8_27
396 R. G. Etkin and E. R. Lebowitz
Research suggests that multiple aspects of into others (Erel & Burman, 1995; Gerard et al.,
family dysfunction may be implicated in the 2006) and threaten youth’s sense of emotional
development of youth anxiety. For instance, security (Davies & Cummings, 1994).
Peleg-Popko and Dar (2001) found that very high It is also likely that bidirectional associations
levels of cohesion (i.e., emotional closeness exist such that youth anxiety elicits problem-
between family members) and low levels of atic responses within family, which in turn con-
adaptability (i.e., ability of the family system to tribute to dysfunction (Minuchin, 1985). For
adjust to situational stressors and developmental instance, withdrawn, nervous, or passive behav-
needs; Olson, 2000) were related to higher levels ior displayed by anxious youth could elicit over-
of anxiety in young children, including specific involved or overprotective parenting that weakens
fears and social anxiety symptoms. Likewise, boundaries and reinforces anxious tendencies
Bögels and Brechman-Toussaint (2006) reported (e.g., Rapee, 2009; Rubin et al., 1999). Youth
findings that highly anxious children (8–12 years anxiety may also contribute to or exacerbate mar-
old) depict greater imbalance in the cohesion and ital problems if parents experience heightened
hierarchy of their families relative to children conflict or disagreement about how to respond to
with average levels of anxiety. A similar picture the anxiety (Ginsburg et al., 2004; Hughes-
emerges from prospective studies as well. Pagani Scalise & Przeworski, 2014), or if the anxiety
et al. (2008) examined trajectories of anxiety and begins to interfere with the degree of quality time
dysfunction over 6 years and found that children parents can spend together or with other family
(4–11 years old) from the highest anxiety trajec- members (Bögels & Brechman-Toussaint, 2006).
tories were 23–31 times more likely to belong to It is also the case that some anxious youth display
the highest trajectory of family dysfunction (i.e., irritable, aggressive, or otherwise disruptive
poor support, communication, acceptance, and behavior, which may contribute to family discord
problem-solving) than to the lowest. Nomura and coercive processes (e.g., Lebowitz et al.,
et al. (2002) found that poor marital adjustment, 2011a; Shimshoni et al., 2019). For instance,
another common indicator of family dysfunction, Tanaka et al. (2010) found that family conflict
was uniquely associated with the development of was associated with high levels of child proactive
youth anxiety (6–23 years), resulting in a four- aggression only for highly anxious youth
fold increase in symptom severity over the course (7–13 years). Authors posit that anxious children
of 10 years. in dysfunctional families may learn to use aggres-
There are multiple theorized mechanisms sion to get their parents to help them, although
explaining associations between these various this strategy likely intensifies the conflict that
aspects of family dysfunction and youth anxiety. contributes to their anxiety. In sum, the nature of
For instance, ill-defined boundaries may increase youth anxiety is such that it may draw out family
youth’s sense of uncertainty about family roles or dysfunction in various ways, and anxiety and
place them in developmentally inappropriate and dysfunction could become mutually reinforcing.
challenging roles, such as being triangulated into
marital conflict (e.g., Hughes-Scalise &
Przeworski, 2014). High degrees of enmeshment Zooming in on Family
or control may promote overreliance on parents, Accommodation
inhibit the development of independence and
autonomy, and decrease opportunities for youth Any discussion of anxiety and family dysfunc-
to experience challenges and develop the coping tion would be incomplete without taking a care-
and self-regulation skills necessary for managing ful look at accommodation. Accommodation
anxiety (Drake & Ginsburg, 2012). Additionally, refers to behavioral modifications or changes
family conflict may directly contribute to stress made by family members that intend to alleviate
and fear, and discord within one family subsys- or avoid a youth’s symptom-related distress.
tem (e.g., the marital relationship) can “spillover” While originally identified and studied
27 Treatment of Youth Anxiety in the Context of Family Dysfunction and Accommodation 397
e xclusively in the context of OCD (Calvocoressi Wu et al., 2016). Settipani and Kendall (2017)
et al., 1995), it is now established that accommo- found that mothers of anxious youth (7–17 years)
dation is highly prevalent within families of presenting to an outpatient clinic indicated that
youth with all anxiety disorders (Lebowitz et al., they would engage in greater accommodation in
2013). Indeed, multiple studies report that that up response to hypothetical vignettes depicting
to 100% of families of anxious youth engage in highly versus minimally distressed children in
some degree of accommodation (e.g., Benito anxiety-provoking situations. When youth pres-
et al., 2015; Kagan et al., 2016; Lebowitz et al., ent with greater anxiety severity, their families
2013, 2015a; Storch et al., 2007; Thompson- may be more likely to feel the need to resort to
Hollands et al., 2014; Zavrou et al., 2019). Most accommodation to reduce distress enough to
data on parental accommodation have focused on facilitate daily functioning. Especially, if the anx-
mothers, but other family members including iety is so severe that it interferes with essential
fathers and siblings also accommodate (Alcan functions that could have serious consequences if
et al., 2021; Lebowitz et al., 2011b). not completed, such as attending school or work,
Examples of family accommodation are families may feel immense pressure to do any-
numerous and varied, but they can generally be thing they can (i.e., accommodate) to ensure
classified into two categories. The first is partici- these functions can take place.
pation in rituals or routines related to the disor-
der. An example is parents excessively showering Relatedly, families accommodate (as they
to alleviate their child’s obsessions about con- respond in other dysfunctional ways) to mini-
tamination and illness (see Lebowitz, 2016). The mize hostile, violent, or coercive behaviors that
second is modification of family functions, such youth may display in the face of their anxiety
as altering schedules, routines, or responsibilities (Lebowitz et al., 2011b, c, 2015b; Zavrou et al.,
because of the youth’s anxiety. These categories 2019). In one study of mothers and youth
are not always distinct; for example, parents may (7–18 years) seeking treatment for OCD,
drive a child to school each day to prevent him/ Lebowitz et al. (2015b) found strong associations
her from worrying about the separation that between coercive–disruptive behaviors and
occurs when taking the school bus, entailing both accommodation frequency, distress, and negative
participation and modification. The specific consequences. In another treatment-seeking sam-
accommodations that families engage in typi- ple of youth with OCD (7–19 years) and their
cally relate to the nature of the anxiety disorder(s). parents, Wu et al. (2014) found that externalizing
For instance, speaking in place of a child is a behaviors predicted distress and negative conse-
common accommodation in families of youth quences associated with family accommodation,
with social anxiety disorder. However, some of controlling for symptom severity, and mediated
the most common accommodations, such as pro- the association between symptom severity and
viding excessive reassurance, are prevalent across family accommodation. McGuire et al. (2013)
disorders (Jones et al., 2015). also found that the magnitude of dysregulation
(emotional, behavioral, and cognitive) displayed
Reasons for Accommodation Several factors by youth (6–17 years) with OCD directly pre-
may influence the degree of family accommoda- dicted family accommodation beyond obsessive-
tion that are not unlike those contributing to fam- compulsive symptom severity. When anxious
ily dysfunction, as described above. One of them youth behave antagonistically, parents may feel
is the severity of youth distress and anxiety that their hand is forced to accommodate in the
symptoms. Meta-analyses find that there is a desired or expected ways, even if doing so nega-
medium effect size for the association between tively impacts the hierarchy or balance of power
greater youth anxiety symptom severity and more within the family and contributes to greater fam-
frequent family accommodation (Strauss, Hale, ily dysfunction.
& Stobie, 2015; Iniesta-Sepúlveda et al., 2021;
Parents’ beliefs and feelings about their child’s worries, parents may inadvertently confirm that
anxiety may also contribute to accommodation. separation is something to be feared and some-
In the study by Settipani and Kendall (2017) and thing that the child cannot cope with. Moreover,
in other studies by Feinberg et al. (2018) and this accommodation prevents the child from con-
Johnco et al. (2022), mothers were more likely to fronting their anxiety and having the opportunity
report that they would engage in accommodation to learn that it will subside or can be handled
if they held greater negative beliefs about their independently. In fact, although most youth
child’s experience of anxiety, including about report feeling less anxious when they are accom-
how harmful it is and their child’s ability to cope. modated and do not want their parents to accom-
Meyer et al. (2018) likewise found that parental modate less, they do not believe that
beliefs about the necessity of accommodation to accommodation will actually help them to feel
prevent youth (7–17 years) from losing emo- less anxious in the future (Lebowitz et al., 2015a).
tional and behavioral control were significantly
correlated with accommodation frequency, even Accordingly, research consistently demon-
controlling for severity of anxiety symptoms. strates the detrimental effects of accommodation
These studies suggest that parents who believe for anxious youth and their families. As noted
anxiety could be harmful to their child might be above, more frequent accommodation is associ-
more likely to accommodate to prevent this ated with greater severity of and functional
potential harm. Seeing a child in distress might impairment associated with youth anxiety and
also exacerbate parents’ own feelings of anxiety OCD symptoms (e.g., Caporino et al., 2012; La
or distress, making them more likely to accom- Buissonnière-Ariza et al., 2018; Storch et al.,
modate (Flessner et al., 2011; Settipani & 2007, 2010). For parents, accommodation is like-
Kendall, 2017). Jones et al. (2015) found accom- wise associated with greater feelings of personal
modation to mediate the association between distress. Accommodation is often quite demand-
mother and child anxiety, suggesting that anxious ing, with most parents engaging in accommoda-
parents may attempt to regulate their own anxiety tions on a daily basis (e.g., Jones et al., 2015;
by accommodating and minimizing their child’s Lebowitz et al., 2013). Certain accommodations
anxiety. This may be especially true when par- may deplete family members’ time and resources.
ents are highly empathetic and thus attuned to For example, a parent who accommodates by
their child’s feelings/distress (Caporino et al., sleeping with his/her child each night may get
2012; Settipani & Kendall, 2017). Taken together, less sleep and have less time to spend with his/her
research suggests that various child and parent partner or other children. In a case study by
factors contribute to the likelihood of problem- Lebowitz and Shimshoni (2018) (further detailed
atic accommodation. below), a mother had to reduce her work hours in
order to accommodate her child’s OCD symp-
The Impact of Accommodation Although toms, which eventually resulted in a loss of fam-
accommodation is generally well-intentioned ily income.
(e.g., parents do not want their child to struggle), Given such outcomes and the amount of strain
research suggests that it is ultimately more accommodation may place on family members,
unhelpful than it is helpful. As depicted in it is easy to see how it could contribute to a
Fig. 27.1, accommodation does tend to “work” broader pattern of family dysfunction. In one
(i.e., alleviate youth anxiety symptoms) in the study of youth with OCD (8–17 years) and their
short term by reducing anxiety or facilitating parents, Peris et al. (2008) found that greater
avoidance. However, in the long term, accommo- family distress when accommodating, and worse
dation maintains or even exacerbates youth anxi- youth consequences in the absence of accommo-
ety by preventing exposure and reinforcing the dation, were associated with more family con-
notion that the child/adolescent can only cope by flict; alternatively, lower levels of distress and
relying on parents. For instance, if parents cancel consequences associated with accommodation

their dinner plans to relieve a child’s separation were associated with higher levels of family
Fig. 27.1 Theoretical

model of the cycle
through which family
accommodation
maintains symptoms of
youth anxiety disorders
cohesion and organization. In the study noted based treatment. In addition to assessing anxiety
above, Wu et al. (2014) similarly found that symptoms, assessment of family functioning
higher levels of accommodation (specifically, may reveal important information about potential
participation in youth OCD symptoms) were sources of difficulty and/or treatment targets.
associated with lower levels of family cohesion, Different aspects of family functioning can be
even controlling for symptom severity. More validly and reliably assessed with both behav-
research is needed to even better elucidate the ioral methods (i.e., family observation tasks) and
associations between accommodation and other questionnaire measures (for one review see
forms of family dysfunction; however, a high Alderfer et al., 2008). The Family Environment
degree of family involvement in a child’s or ado- Scale (Moos, 1994), for example, measures dif-
lescent’s symptoms will likely lead to blurred ferent domains of family (dys)function (e.g.,
boundaries and alterations of typical family cohesion, control, conflict) and has been widely
structures/roles. It is also likely that families used including in studies investigating the course
who already struggle with boundaries and con- and treatment of youth anxiety and OCD (e.g.,
flict may be more likely to accommodate because Peris et al., 2012).
they have less of a foundation for taking the In terms of assessing accommodation specifi-
often-harder route of not accommodating. cally, there are several available parent- and
Although these ideas remain to be tested empiri- youth-report and clinician-rated measures. The
cally, at present the research clearly suggests that
Family Accommodation Scale (FAS) was the first
severe accommodation incurs difficulties for measure of accommodation, developed for fami-
youth, parents, and the family system alike. lies of individuals with OCD (Calvocoressi et al.,
1995). Lebowitz et al. (2013) later modified this
measure to create the Family Accommodation
Evidence-Based Assessment Scale – Anxiety (FASA), which is a 13-item
parent- report measure that assesses family
Before discussing intervention approaches, it is accommodation for all anxiety disorders. The
necessary to touch on evidence-based assess- FASA total score consists of nine items measur-
ment, which lays the groundwork for evidence- ing the frequency of accommodation in terms of
participation (e.g., “Have you avoided doing and parent-report total scores (r = 0.54; Lebowitz
things, going places, or being with people et al., 2015a).
because of your child’s anxiety?”) and modifica- The development of several other measures of
tion (e.g., “Have you modified your family rou- family accommodation have followed. The
tine because of your child’s symptoms?”). These Family Accommodation Checklist and
items are rated on a 5-point scale (ranging from 0 Interference Scale (Thompson-Hollands et al.,
“never” to 4 “daily”) with higher total scores 2014) is a parent-report measure that assesses the
indicating more frequent accommodation frequency and interference of 20 specific accom-
(range = 0–36). The four remaining items assess modation behaviors. The Pediatric
parental distress associated with accommodation Accommodation Scale (Benito et al., 2015) is a
(i.e., “Does helping your child in these ways 14-item clinician-rated measure that assesses the
cause you distress?”) and consequences of not frequency, severity, and impact of accommoda-
accommodating (e.g., “Has your child become tion; there is also a corresponding 5-item parent-
distressed when you have not provided assis- report measure. The Parenting Anxious Kids
tance? To what degree?”). Research has found Ratings Scale (Flessner et al., 2017) is a 32-item
the FASA to have good psychometric properties, parent-report measure consisting of five factors
including internal consistency (αs = 0.87–0.91; that assess the degree of conflict, overinvolve-
Lebowitz et al., 2013, 2019b), test–retest reliabil- ment, accommodation, modeling, and emotional
ity (r = 0.79; Lebowitz et al., 2019b), convergent warmth/support within the family. Finally, the
and divergent validity (i.e., with measures of Parental Accommodation Scale (Meyer et al.,
anxiety and depression), and factorial structure 2018) is a 12-item parent-report measure that
(i.e., two factors representing participation and assesses the frequency of and beliefs about
modification, established by exploratory and accommodation. Each of these measures has ini-
confirmatory factor analyses; Lebowitz et al., tial evidence of satisfactory psychometric
2013, 2019b). properties.
The FASA also has a youth self-report version
(FASA-CR; Lebowitz et al., 2015a). Like the par-
ent version, nine items forming the total score Evidence-Based Treatment
assess the frequency of accommodation (e.g., Approaches
“How often did your parent help you avoid things
that make you feel anxious?”) and four items Research over the past several decades reveals
assess associated distress and consequences. The impressive advances in available efficacious,
FASA-CR has three additional items that assess evidence-based treatment approaches for youth
beliefs about accommodation and its efficacy anxiety and OCD (Freeman et al., 2014; Higa-
(“When my parent helps me in this way, I feel McMillan et al., 2016). Of course, there is vari-
less anxious”; “If my parent continues to help me ability in the number of youth who respond to
in these ways, I will feel less anxious in the such treatments (e.g., 46–79% diagnostic recov-
future”; “I believe my parent should help me less ery; Silverman et al., 2008), which may be attrib-
in these ways, when I’m anxious”). The utable to many factors. For example, in many
FASA-CR (total score) has evidence of satisfac- cases the anxiety itself and comorbid difficulties
tory internal consistency (α = 0.79–0.85; (e.g., oppositional behaviors or depressive symp-
Lebowitz et al., 2015a, 2019b), test–retest reli- toms) may directly interfere with the therapeutic
ability (r = 0.52; Lebowitz et al., 2019b), conver- process (e.g., Garcia et al., 2010). The degrees of
gent validity (i.e., significant associations with family (dys)function and accommodation are
other anxiety measures), and factorial structure. additional factors that may hinder or support
There is moderate agreement between the youth- treatment progress (e.g., Ginsburg et al., 2008).
With regard to the latter, Peris et al. (2012) Cognitive-Behavioral Therapy (CBT)
found that higher family cohesion predicted bet- with Family Involvement
ter treatment outcomes for youth (8–17 years)
with OCD, and Crawford and Manassis (2001) Variants of CBT have been developed that involve
found that greater family dysfunction and parent- parents or families to varying degrees (e.g., attend
ing stress predicted less improvement over the part of every session or a few supplementary ses-
course of treatment for children (8–12 years) sions) and generally focus on psychoeducation
with anxiety disorders. Kagan et al. (2016) found and skill-building that might bolster youth’s
that pretreatment levels of accommodation were treatment progress (Barmish & Kendall, 2005).
associated with higher clinician severity ratings For example, in the first randomized controlled
of the youth’s (6–17 years) anxiety following trial (RCT) to test the efficacy of CBT for anxiety
treatment. Garcia et al. (2010) also found that with parent involvement, Barrett et al. (1996)
family accommodation predicted treatment out- compared individual CBT to CBT with Family
comes for youth (7–17 years) with OCD, such Anxiety Management (FAM), and to a waitlist
that those with lower initial levels of family condition, in a sample of youth with anxiety dis-
accommodation showed greater improvement orders and their parents (N = 79, 7–14 years). In
over the course of psycho- or pharmacotherapy. the FAM condition, parents learned behavior
Merlo et al. (2009) found that decreases in family management techniques, strategies for recogniz-
accommodation over the course of intensive or ing and regulating their own emotions in response
weekly family-based cognitive-behavioral ther- to their anxious child, and skills such as problem-
apy (CBT) predicted better youth outcomes solving and communication. While both CBT
(6–18 years), even controlling for baseline levels and CBT+FAM were associated with significant
of OCD severity and impairment. improvements in youth anxiety symptoms, a
These findings may be explained by the notion greater percentage of youth from the CBT+FAM
that families who are highly dysfunctional and condition were diagnosis-free following treat-
engage in frequent accommodation might have ment (84% vs. 57%) and at the 6-month (84% vs.
more difficulty supporting their children in 71%) and 12-month follow-ups (95% vs. 70%).
follow-through with treatment, such as engaging To date, however, the study by Barrett et al.
in exposures. Likewise, high levels of family (1996) is something of an outlier in showing that
accommodation, and potentially other dysfunc- treatment with family involvement has benefits
tional processes like enmeshment, may directly above and beyond individual child CBT (for
undermine treatment (e.g., by preventing expo- another exception, see Cobham et al., 2010). On
sures or reinforcing anxious beliefs) or youth’s the surface, this pattern of results is puzzling
motivation to seek or engage in it (e.g., because given families’ clear role in youth anxiety.
they can rely on parents instead of needing to However, there are many possible reasons why
cope) (Lebowitz et al., 2019a; Lebowitz & most parent- and family-involved treatments may
Shimshoni, 2018). not have added benefit. Some of these may be
Although family dysfunction and accommo- methodological in nature, such as limited inclu-
dation are thus poor prognostic indicators, they sion of relevant outcomes measures, or insuffi-
are “tractable” issues that can be ameliorated cient power to detect for whom these treatments
within the context of treatment (Lewin, 2014). work best (e.g., Caporino & Storch, 2016). Other
We next describe evidence-based treatment potential reasons may relate more to the theoreti-
approaches for youth anxiety disorders and OCD cal models guiding the parent involvement. For
that directly target family dysfunction and instance, the aforementioned treatments focus
accommodation as a means of improving treat- either on training parents as lay CBT therapists or
ment outcomes. The two general approaches on teaching parents’ skills, such as emotion regu-
include CBT with parent or family involvement, lation and problem-solving, and may not address
and parent-guidance.
the most salient aspects of family dysfunction 94%; ST: 82%) retained this status at the 3-month
that have been found to maintain youth anxiety. follow-up. As in the pilot study, the families who
A few treatment approaches address this limi- participated in PFIT demonstrated significant
tation. One notable example is Positive Family improvements in accommodation and conflict, as
Interaction Therapy (PFIT), which is a six- well as family cohesion, compared to those fami-
session flexible treatment module designed spe- lies who had received ST only.
cifically for families with complex dysfunction to Hughes-Scalise and Przeworski (2014) also
serve as an adjunct to standard therapy (i.e., indi- discuss an approach to treating OCD and comor-
vidual CBT) (Peris & Piacentini, 2013). PFIT is bid oppositional defiant disorder (ODD) vis-à-vis
set apart from the treatments described above in improving dysfunctional family processes in one
that it emphasizes psychoeducation and skills notable case study of a 7-year-old boy and his
that relate specifically to the role of the family in family. Clinicians identified several dysfunc-
OCD, and how family dynamics may undermine tional family processes at the outset of treatment,
youth’s engagement in therapy. The psychoedu- including enmeshment, marital conflict (and tri-
cation component of PFIT includes information angulation into the conflict), and poor communi-
about the different ways that families accommo- cation, that they deemed imperative to address
date, how it maintains symptoms, and what for the child to successfully engage in/benefit
makes it difficult to disengage from. Families are from treatment. As such, in addition to conduct-
taught to how to notice and track their emotions ing CBT with the child, clinicians also drew upon
in response to their child’s or adolescent’s OCD principles of family systems theory to improve
symptoms and practice skills for emotional regu- boundaries, alignment, and hierarchy within the
lation, distress tolerance, problem-solving, and family (e.g., by helping parents reframe each
disengaging from accommodation. Families also other’s behavior, role-play and resolve dysfunc-
learn how to complete a functional analysis of tional interactions, implement appropriate conse-
difficult situations related to the child’s/adoles- quences for the child’s disruptive behaviors). Due
cent’s OCD and engage in exercises designed to to the severity of both the family dysfunction and
promote positive family processes (e.g., child symptoms, treatment lasted 18 months with
cohesion). two sessions per week at times (i.e., one focused
In the pilot study for this treatment, 20 youth on CBT, one focused on parent work). However,
with OCD (8–17 years) and their families ultimately with this approach, the child and fam-
received either manualized CBT with weekly ily showed significant improvement (e.g., symp-
psychoeducational check-ins with parents (i.e., toms in subclinical range on standardized
standard treatment; ST) or ST but with PFIT measures; appropriate hierarchy of authority
instead of the weekly parent psychoeducation. established within the family).
Following treatment, remission rates were 50%
for the youth of families who received PFIT com- Summary of the Extant Research on CBT
pared to 20% for the youth who received with Family Involvement Although consider-
ST. Gains for both conditions were maintained able research reveals associations between family
3 months later. Families who received PFIT also functioning and youth anxiety, incorporating par-
showed significant decreases in family accom- ents or families into anxiety treatment does not
modation, conflict, and blame compared to those always have the expected positive effects (e.g.,
who received only ST. Subsequently, the efficacy Barmish & Kendall, 2005). Treatments that
of these two treatment conditions was evaluated involve families by teaching specific and person-
in an RCT of 62 youth with OCD (ages 8–17) and alized skills to reduce dysfunction and
their families (Peris et al., 2017). Following treat- accommodation that may be maintaining symp-
ment, 58% of youth whose families had received toms or interfering in treatment progress may be
PFIT achieved remission compared to 27% of most effective, as compared to treatments that
youth who received ST; almost all youth (PFIT: focus on general parenting skills and psychoedu-
cation. Family involvement in youth treatment driven. The basis for targeting youth anxiety
may also be most indicated and effective for through changing parent behavior derives from
those families who struggle with high levels of attachment theory, which posits that the close
dysfunction, and may not be useful for all fami- emotional bond between youth and parents leads
lies of anxious youth (Peris & Piacentini, 2013). youth to seek and parents to provide soothing or
protection in the face of distress such as anxiety
Additional research is needed to identify (Lebowitz et al., 2014a). SPACE is also informed
mechanisms of change in these treatments with by principles of nonviolent resistance (Lebowitz
family involvement; specifically, to determine et al., 2014a; Omer & Lebowitz, 2016), namely,
whether changes in family function or processes the utility of enacting one’s own beliefs and val-
account for decreases in youth anxiety (Silverman ues instead of directly trying to change another
et al., 2019; Van der Giessen et al., 2019). person’s behavior. Guided by these concepts,
Additionally, although direction of effects is SPACE teaches parents how to help youth cope
rarely examined in treatment outcome studies with their anxiety by acting unilaterally to
(Silverman et al., 2009), improvements in youth respond to anxiety in ways that are supportive but
anxiety might positively benefit family function, not accommodating. The specifics of this treat-
even if families are not directly involved in treatment are described next.
ment (e.g., if youth are less anxious, families
experience less conflict and engage in less Treatment Overview SPACE is an eight-part
accommodation; Kagan et al., 2016). Finally, manualized treatment that can be individually
these treatment approaches do not consider tailored and delivered flexibly, typically within
whether family involvement without youth 10–12 sessions. The first part of treatment centers
involvement could result in meaningful gains. on explaining the concept of anxiety with a focus
This limitation is addressed with the treatment on its interpersonal nature. Emphasis is placed on
approach described next. discussing the ways that anxiety leads youth to
rely on parents and can weaken boundaries within
the family. The first part of treatment also high-
Parent-Guidance: SPACE lights the rationale for parent-based treatment
and why past attempts to directly change the
SPACE (Supportive Parenting for Anxious child’s anxiety have not worked, setting the stage
Childhood Emotions; Lebowitz et al., 2014a) is a for unilateral action on the part of the parent(s). A
parent-only treatment for youth anxiety disorders central technique that is introduced is responding
and OCD that addresses many of the barriers to supportively to the child’s anxiety. Support is
and limitations of other individual and family- characterized by acknowledging, validating, and
involvement treatments. Despite being a com- normalizing the child’s anxiety while also
mon treatment modality for externalizing expressing confidence in their ability to cope and
disorders, parent-only approaches for treating manage difficult feelings independently.
youth anxiety are rare, and limited in various Supportive responses are contrasted to ones that
ways (e.g., appropriate for a limited age range, are less effective due to being too demanding
only evaluated in open trials; Cartwright-Hatton (e.g., telling a child to “get over” their fear, or
et al., 2005; Thirlwall et al., 2013). SPACE, in that there is nothing to be afraid of) or protective
contrast, is appropriate for the treatment of a (e.g., validating a child’s fear but also their need
wide age-range of youth with any primary anxi- to avoid feeling scared). Parents are instructed in
ety disorder or OCD and does not necessitate the how to form supportive statements and
youth’s direct participation or collaboration in encouraged to use them in response to their
treatment (e.g., agreeing to try CBT techniques). child’s anxiety.
SPACE also stands out from other treatments
in that its rationale and techniques are theory-
The concept of accommodation is introduced that might arise in response to parental changes,
in the second part of treatment. Families gain without being drawn into a conflict or power
insight into why accommodation occurs and how struggle or reverting to accommodation. These
it inadvertently maintains youth anxiety and reli- modules can be introduced at any point in treat-
ance on parents, and work with the therapist to ment, or not at all, depending on each family’s
chart all the ways they accommodate. The needs.
remainder of treatment focuses on systematically
decreasing accommodation while continuing to Supporting Research In an initial pilot study of
increase support. Parents are guided in develop- SPACE conducted with parents of youth with pri-
ing plans to reduce specific accommodations, mary anxiety disorders (N = 10, 9–13 years),
with parents taking increasing ownership of this Lebowitz et al. (2014a) found that 60% of youth
process as treatment progresses (parts three responded to treatment based on posttreatment
through seven). For instance, a plan to reduce the scores on the Clinical Global Impressions Scale
accommodation of providing excessive reassur- (CGI; ratings of “much” or “very much
ance might entail parents only responding one improved”) and Pediatric Anxiety Rating Scale
time with a supportive statement and then remain- (average change in symptom severity of 38.4%).
ing quiet. The plan would not entail telling the In addition, there were significant reductions in
child to limit their reassurance-seeking, as this family accommodation following treatment (as
would necessitate their collaboration and align measured by the FASA), and client satisfaction
with a demanding instead of supportive stance. was extremely high. Subsequently, Lebowitz
Parents are coached in using written communica- et al., (2019a) conducted an RCT comparing
tion to announce these plans to the child, which SPACE to individual child CBT (with an empha-
in addition to increasing clarity and avoiding sis on behavioral exposures) in a sample of youth
miscommunicating (e.g., due to parent or child with primary anxiety disorders and their parents
emotions during the encounter) allows parents to (N = 124, 7–14 years). Youth in both conditions
express their intent to act without getting drawn showed significant improvement on symptom
into potentially dysfunctional interactions. The questionnaires and the CGI. Families in both
final part of treatment involves reviewing youth conditions also showed equivalent reductions in
progress and changes in parental attitudes and parenting stress and were equally satisfied with
skills, and planning for additional goals and/or the treatment they received. Although family
relapse prevention. accommodation significantly declined following
In addition to the eight parts of treatment, treatment for both conditions, this change was
SPACE contains four supplementary session significantly greater for families who received
modules that provide parents with tools for cop- SPACE.
ing effectively with various forms of dysfunction
that can arise during treatment or impede its There is also preliminary evidence that SPACE
progress. One module focuses on increasing is beneficial for the treatment of youth diagnosed
parental collaboration by identifying and resolv- with primary OCD from a small pilot study
ing sources of disagreement parents may have in (Lebowitz, 2013) and case study (Lebowitz &
addressing the child’s anxiety or implementing a Shimshoni, 2018). The pilot study included par-
plan. Another module teaches parents how to ents of six children who refused participation in
recruit and engage individuals from outside of CBT. Following 10 weeks of SPACE, parent-
the nuclear family to serve supportive functions, reported family accommodation and child OCD
ranging from reinforcing the child’s progress to symptoms and coercive–disruptive behaviors
aiding in a plan to reduce accommodation to showed significant reductions compared to
helping in the face of difficult child behaviors. pretreatment scores. The case study involved

The remaining two modules address how to man- treatment of a 13-year-old White girl with obses-
age threats of self-injury and disruptive behaviors sions and compulsions related to a fear of harm-
ing a person of color. Severe and pervasive family mantling the different elements of treatment and
accommodation and dysfunction was docu- the impact they have on youth anxiety and family
mented at the outset of treatment. Throughout functioning. Future studies could also compare
12 weeks of SPACE, parents were able to disen- SPACE with additional treatment conditions,
gage from accommodations that were maintain- including other parent-based or family-
ing the child’s symptoms, such as participating in involvement approaches, to provide further sup-
a bedtime routine involving repeated reassurance, port for its efficacy.
not inviting others to the home, driving the child
to school, and hiding knives/cutting food for the
child. Following treatment, the child no longer Future Directions
met criteria for an OCD diagnosis based on par-
ent- and child-reports on the Anxiety Disorders A long history of research speaks to the impor-
Interview Schedule and significant reductions on tance of considering family functioning in under-
standardized symptom measures. standing the development and informing the
treatment of youth anxiety. Despite this wealth of
Summary of the Extant Research on knowledge, gaps in the literature are evident.
SPACE Despite research indicating that accom- There is a need for longitudinal studies of accom-
modation can impede treatment engagement and modation to confirm hypothesized bidirectional
progress, in most youth anxiety treatments, par- effects with anxiety symptoms over time (see
ents are included as consultants or co-clients, and Bertelsen et al. 2022, for a recent notable exam-
change in parenting behavior/family functioning ple). Additionally, few studies have simultane-
is not the central focus (Forehand et al., 2013). ously included indices of accommodation and
SPACE focuses on the ways that parents can help other forms of family dysfunction, limiting
youth overcome their anxiety and OCD exclu- understanding of how they are related (for nota-
sively by changing their own behavior and in so ble exceptions, see Peris et al., 2008; Wu et al.,
doing, improving family boundaries and dynam- 2014). For example, future research could exam-
ics. SPACE importantly and uniquely provides ine the co-occurrence of accommodation and
parents with specific guidance on reducing other processes that may adversely impact or
accommodation, which differs from other treat- result from poor family boundaries (e.g., enmesh-
ments that, at most, incorporate psychoeducation ment). Such findings could be important to
or general guidance about accommodation and informing family-based intervention efforts or
the importance of reducing it (e.g., Freeman understanding their potential mechanisms (e.g.,
et al., 2003; Kagan et al., 2016; Merlo et al., reducing accommodation could lead to youth
2009). anxiety remission vis-à-vis improved family
functioning).
Given that SPACE has initial evidence of At present, SPACE is the only empirically
being as effective as individual CBT for treating supported treatment that has the main goal of
youth anxiety, it may be an excellent option for reducing family accommodation and does not
cases in which youth will not directly engage in require youth participation. Other treatment
treatment. It may also be an excellent fit for fami- options for improving symptoms via reducing
lies who experience high levels of dysfunction family dysfunction have exclusively targeted
given its focus on deescalating conflict and disen- youth with OCD and are designed to be imple-
gaging from coercive process without compro- mented alongside or adjunct to child-based treat-
mising treatment goals; however, its efficacy for ment (e.g., PFIT). In the future, these approaches
this purpose remains to be empirically tested. As could be adapted to serve as stand-alone
with the cognitive-behavioral approaches treatments involving parents only. It could more-
described above, future research on SPACE could over be tested whether they are appropriate and
examine treatment mechanisms or focus on dis- effective for all youth anxiety disorders, given
their higher incidence than OCD (Merikangas to better understand which youth may most ben-
et al., 2010), and given that accommodation and efit from such family-based treatment approaches
dysfunction can be just as prevalent in the context and how such approaches work to alleviate
of anxiety disorders (e.g., Lebowitz et al., 2014b). symptoms.
Future research could also investigate addi-
tional positive and negative prognostic indicators
of the treatments described in this chapter. As an References
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Parent Training for Childhood
Anxiety 28
Adam B. Lewin and Kelly Kudryk
The “dry-cleaning model” of child anxiety treat- Rationale for Parent Inclusion
ment is unfortunately a myth – it is unreasonable
to expect that a child’s anxiety disorder will be suf- Insufficient Improvement from Current
ficiently treated by dropping a child off with a Interventions The rationale for parental inclu-
therapist, regardless of the clinician’s skill. Family sion in the treatment of childhood anxiety is
change and support is a critical component in the multifaceted. Despite the efficacy of current
treatment of child and adolescent anxiety. first-line treatments for childhood anxiety disor-
Etiological models suggest that parenting behav- ders, namely individual cognitive-behavioral
iors impact child anxiety (Hudson & Rapee, 2001). therapy (CBT) and selective serotonin reuptake
However, the optimal role of parents in the treat- inhibitors (SSRIs), these interventions yield only
ment of children with anxiety disorders is unclear. modest improvement (Eisen et al., 2008). For
What parent-training strategies are helpful for alle- example, the Child–Adolescent Anxiety
viating childhood anxiety? Is parent training a key Multimodal Study (Walkup et al., 2008) pro-
treatment component or is it ancillary? Are there duced only a 59.7% improvement rate in anxiety
benefits to parent therapy, e.g., anxiety manage- symptoms following a meticulously imple-
ment training? What is the efficacy of applying mented CBT protocol (the Coping Cat protocol;
non-anxiety-specific behavioral parent-training Kendall & Hedtke, 2006). When the outcome of
approaches, such as those employed for disruptive treatment is based on a “diagnosis-free” crite-
behavior disorders? While the answers are far rion, results are slightly less encouraging (56.5%
from unambiguous, this chapter will: (1) discuss diagnosis-free based on meta-analytic tech-
the rationale for parent training and parental niques) (Cartwright-Hatton et al., 2004).
involvement in psychotherapy for child anxiety, Treatment responses may be even lower in com-
(2) review research in this developing area, and (3) munity samples where patient presentation is
discuss limitations in the extant research and rec- more heterogeneous and implementation of
ommendations for practice and future study. treatment is less standardized (Weisz et al.,
1992). Given that as many as 50% of youth
A. B. Lewin (*) · K. Kudryk remain symptomatic following an adequate trial
Department of Pediatrics, University of South Florida of child-focused CBT (in the absence of signifi-
Rothman Center for Neuropsychiatry, St. Petersburg, cant parental participation) (Ginsburg &
FL, USA
e-mail: alewin@usf.edu; Schlossberg, 2002; Wood et al., 2006), family-
kelly.kudryk@psych.utah.edu based approaches are worthy of consideration.
https://doi.org/10.1007/978-3-031-14080-8_28
412 A. B. Lewin and K. Kudryk
Family Transmission of Anxiety The heritabil- their child’s exposure to stressful stimuli, perhaps
ity of anxiety disorders must also be considered because they are fearful that the child will lack an
when developing and implementing treatment. ability to cope. However, despite the best of
Anxious children are more likely to have anxious intentions, inadvertent and intentional strategies
parents – data from family aggregate and genetic to mitigate a child’s exposure to anxiety may
studies suggest a range from 60% to 80% backfire. First, overprotection (among parents of
(Chorpita & Barlow, 1998; Ginsburg & anxious youth) is often accompanied by critical
Schlossberg, 2002; Hudson & Rapee, 2001; Last and controlling parental behavior (Cobham et al.,
et al., 1987; Pauls, 2008; Rutter et al., 1990). For 1998; Eisen et al., 2008; Hudson & Rapee, 2001;
example, Beidel and Turner (1997) examined Messer & Beidel, 1994; Siqueland et al., 1996).
129 school-aged children (7–12 years) and found At times, parental responses to an anxious child’s
that 33% children of parents with an anxiety dis- symptoms may even be harshly antagonistic
order met criteria for an anxiety disorder whereas (Renshaw et al., 2005). Second, in comparison to
only 9% of children of normal controls met crite- youth without anxiety, anxious youth describe
ria for an anxiety disorder. Both genetic and envi- their parents as less supportive, less warm, and as
ronmental (learned) mechanisms are likely granting less psychological autonomy (Chorpita
involved in multigenerational transmission of & Barlow, 1998). Third, the development of psy-
anxiety (Hettema et al., 2001; Rapee, 1997). chological autonomy may be hindered by over-
protection, control, and punishment of
independence (Hudson & Rapee, 2001). For
Family-Based Maintenance of Anxiety Parents example, when parents reinforce anxious
may model avoidant behavior as well as anxious responding and attempt to manage all of the
thinking patterns (e.g., excessive reassurance, stress in a child’s environment, the youngster’s
distorted cognitions, though-action fusion) to an development of adaptive behaviors for coping
impressionable child (Capps & Ochs, 1995; with anxiety may fail to develop (e.g., emotion-
Dadds et al., 1996; Eisen et al., 2008; Moore focused coping) (Spence, 1994; Strauss et al.,
et al., 2004). In a review of the literature, Ginsburg 1987). Further, children may receive insufficient
and Schlossberg (2002) suggest that parents of exposure to learning paradigms involving stress-
anxious youth (in comparison to parents of non- ful situations. By shielding a child whenever
anxious youth) are (1) more likely to interpret stress is encountered, parents may communicate
ambiguous situation as worrisome/stressful and a message suggesting that the child is incapable
(2) more supportive of avoidance-based coping of handling anxiety. Finally, parents of anxious
strategies. Moreover, parents may strengthen youngsters are more likely to exhibit behaviors
(i.e., reinforce) the likelihood of anxiety-related that communicate a greater perception of threat
behaviors via escape, avoidance, attention, and in the child’s environment (Barrett et al., 1996;
accommodation of behaviors (Barrett et al., 1996, Dadds et al., 1996; Spence et al., 2000). In a vis-
2001; Geffken et al., 2006; Kendall et al., 2008; cous cycle, parental overprotection and
Last et al., 1987; Lewin & Piacentini, 2010; communication-of-environmental-threat may
Meiser-Stedman et al., 2005; Smith et al., 2007; reinforce the child’s anxious thoughts and
Wood et al., 2002). Parent-focused intervention behaviors.
can decrease the likelihood of child anxiety in the Although longitudinal research suggests that
shorter term, ~12 months (Cartwright-Hatton aforementioned parental behaviors maintain
et al., 2018; Ginsburg et al., 2015) but not in the child anxiety (Lieb et al., 2000), the relationship
longer term, 6 years (Ginsburg et al., 2020). between child anxiety and parent anxiety is recip-
rocal (Bögels & Siqueland, 2006; Chorpita &
Parents of anxious youngsters are often over- Barlow, 1998; Kendall et al., 2008) and thus even
protective (Last & Strauss, 1990). It is not non-anxious parents may be conditioned to
uncommon for anxious parents to attempt to limit exhibit behaviors associated with the p roliferation
28 Parent Training for Childhood Anxiety 413
of child anxiety (Manassis & Bradley, 1994). In their child to generalize therapeutic procedures to
other words, both parents and children contribute other environments.
to anxiety-maintaining factors, e.g., control, criti-
cism, conflict, and overprotection (Bögels & In summary, family aggregation (or hereditary
Melick, 2004). Notably, changes in family func- predisposition), in combination with several par-
tioning variables are related to long-term treat- enting factors, likely plays a significant role in
ment outcomes for anxious youth (Crane et al., the development and maintenance of child anxi-
2021), suggesting the importance of treating the ety. Further, modeling and reinforcement of anx-
family unit to maintain changes produced from ious behaviors, overprotection, conflict, and
intervention. verbal/nonverbal communication (suggesting
that the world is unsafe and that the child is ill-
Bolstering Compliance Cognitive-behavioral equipped to cope) can impede treatment (Nauta
therapy for anxiety disorders requires intensive et al., 2003; Spence et al., 2000). Moreover, chil-
practice in and out of treatment sessions (Kendall dren may lack the initiative and/or their anxiety
& Hedtke, 2006; Lewin et al., 2005a or b; March may be too pervasive for them to participate in
& Mulle, 1998; Piacentini et al., 2007; Silverman therapy independently. Consequently, it is not
et al., 1999). Parent endorsement and support for unlikely that child-focused therapies will be
treatment procedures are paramount in compli- unsuccessful (Thienemann et al., 2006).
ance with therapeutic procedures outside of ses- Accordingly, the addition of parent training and
sion (Hudson & Kendall, 2002). Just as it is family interventions targeting anxiety-
unrealistic to expect many children to complete maintaining behaviors may improve outcomes
homework from school without some level of (Ginsburg & Schlossberg, 2002; Lewin et al.,
parental attention/supervision, one cannot rely on 2005a; Spence et al., 2000; Thienemann et al.,
youngsters to engage in CBT exercises (e.g., cog- 2006).
nitive logs, exposure/response prevention, rou-
tine modifications) without parental assistance.
Moreover, the most potent aspect of CBT for Parent-Training Approaches
child anxiety – exposure – can be terrifying and for Youth with Anxiety
counterintuitive to a child. Exposures involve, in
a hierarchical fashion, presentation with (in vivo Despite nearly universal agreement for the neces-
or imaginally) a feared stimuli or situation. sity of parent involvement in the treatment of
Moreover, the child is asked to reframe from youngsters with anxiety disorders, there is a wide
using their established (though ultimately fear- variability in approach and application. Ginsburg
maintaining) repertoire of coping strategies (e.g., and Schlossberg (2002) noted that the content of
avoidance, escape, ritualization, and reassurance parent-focused interventions typically included
seeking). Not surprisingly, children are often psychoeducation, contingency management, and
less-than-excited about participation in therapeu- parental inclusion in treatment.
tic exposures. When a child is fearful about
engaging in therapeutic exercises (and perhaps Psychoeducation Parent psychoeducation is a
doubtful of the potential benefit, especially in the critical aspect of treatment for anxious youth
initial stages of treatment), it is unrealistic to (Lewin et al., 2005b). Although psychoeducation
expect independent engagement in exposure- is often disorder specific, the omnibus goal is to
based practice. Consequently, parental endorse- provide a cognitive-behavioral conceptualization
ment of the treatment is critical. This is especially for the manifestation and treatment of anxiety
important when a child’s motivation is low, (Ginsburg & Schlossberg, 2002). Parental educa-
insight is poor, and expectation for improvement tion should highlight the biological etiology of
is minimal. Thus, experts may advocate training anxiety with a goal of reducing parental self-
parents to participate in session and assisting blame (or child blame) for the development of a
child’s anxiety. Nevertheless, the role of the Hedtke, 2006; March & Mulle, 1998), to partici-
child’s environment (e.g., the family) in main- pation throughout therapy (Lewin & Piacentini,
taining anxiety must be emphasized. The thera- 2010; Smith et al., 2007), to training as a lay-
pist might explain to the parent that trying to therapist (Hahlweg et al., 2008; Thienemann
provide comfort and protection, despite being et al., 2006). Silverman et al. (1999) described a
innate parental responses, may worsen symptoms model where the therapist’s responsibilities are
in an anxious child. Subsequently, the therapist gradually transferred to the parent. Certain fac-
should impart knowledge regarding the therapeu- tors may contraindicate parent assumption of
tic techniques that will be used to extinguish therapeutic roles. High parental anxiety, caustic
anxiety and augment adaptive coping skills. parent–child interactions, poor child motivation,
Additionally, education may focus on the tripar- and/or oppositional child behavior dictates con-
tite model (Lang, 1979) to assist parents under- current or precursor interventions.
stand and recognize relations between
physiological symptoms, anxious thoughts, and Contingency Management Contingency man-
avoidant behaviors. For example, educating a agement techniques are commonly included as
parent that picking up a child (with a stomach- part of parent training for child anxiety disorders.
ache) the day of the child’s exam might actually Contingency management (often called behav-
proliferate anxiety. ioral parent training) involves teaching parents
operant principles including: (1) positive rein-
For psychologically minded parents, espe- forcement (e.g., rewarding participation in treat-
cially in family systems where coercive cycles ment); (2) negative reinforcement (eliminating
are minimal, psychoeducational aspects of parent escape and avoidance as coping strategies); (3)
training may be sufficient for training the parent extinction (ignoring reassurance seeking behav-
to begin to model appropriate behavior and dis- ior); and (4) punishment (e.g., removal of privi-
continue reinforcement of behavior/overprotec- leges or the presentation of a time-out following
tion that may perpetuate the child’s anxiety. oppositional behavior). Contingency manage-
However, at the very least, parent training should ment techniques can target anxiety specifically or
attempt to create an anxiety-neutral environment. general behaviors (e.g., cooperation, remaining
For parents, psychoeducation may open the first on-task, compliance with assignments). Training
window into the pervasive and debilitating nature should include learning how to identify rewards
of their child’s anxiety (Engel et al., 1994; Yeh & (that can be used to increase desired behaviors).
Weisz, 2001). Further, this training can provide An emphasis is placed on avoiding power-
the essential “sales pitch” to the parent for treat- struggles with the child by (1) being consistent,
ment; as discussed above, the child is unlikely to (2) following-through with contingencies, and
“buy-in” to treatment without parental (3) refraining from emotionally reactive
endorsement. responses to the child. Implementing contin-
gency management techniques can dramatically
Training in Therapeutic Techniques Parent shift family roles (from child control (or anxiety-
training for youth with anxiety disorders often mediated control) to parent control). Despite
involves instructing a parent to participate with emotions (e.g., anger, worry, frustration) that a
child-focused therapeutic exercises in-and- parent or child may be experiencing when deliv-
outside of session (Barrett et al., 2008; Ginsburg ering/receiving a consequence (e.g., a timeout) or
& Schlossberg, 2002; Silverman et al., 2008; conducting a therapeutic exposure exercise (e.g.,
Thienemann et al., 2006). Training ranges from withholding reassurance to a child’s anxious
teaching the parent to monitor and assist with request), the parent should give the perception of
therapeutic homework as needed (Kendall & control and level-headedness. The parent should
strive to project confidence in the techniques and Treatment Studies

control over the situation. Parent and child emo-
tional reactions (to potentially major role As mentioned earlier, child-based anxiety treat-
changes) can be discussed in session. These tech- ments have produced modest results. To improve
niques are commonly included for most child outcomes, researchers have examined whether
anxiety disorders including obsessive-compulsive parent involvement enhances child-based treat-
disorder (OCD) and posttraumatic stress disorder ments for childhood anxiety. Many studies have
(PTSD) (Barrett et al., 1996; Carr, 2004; Dadds compared CBT for child anxiety with and with-
et al., 1991; Lewin et al., 2005b; Smith et al., out significant parental components. It is impor-
2007; Wood et al., 2006). tant to note that the format of treatment, amount
of parent involvement, and parent-training con-
Additional Strategies Other ancillary parent- tent varies between studies (see Table 28.1).
training approaches may include parent anxiety Some have reported parent inclusion to be supe-
management, family problem-solving, and com- rior (Barrett et al., 1996; Wood et al., 2006), but
munication training (e.g., interventions aimed at most found that CBT with parent involvement
improving parent–child interactions). Typically, did not outperform child-only CBT (Kendall
these strategies do not focus on the specific par- et al., 2008; Nauta et al., 2003; Öst et al., 2001).
enting practices that are hypothesized to contrib- Meta-analyses have concluded the same: no sig-
ute to anxiety development and maintenance nificant differences in treatment outcomes
(Wood et al., 2006). Consequently, these (Carnes et al., 2019; Reynolds et al., 2012).
approaches are normally applied only when the There is some evidence suggesting that, non-
characteristics of a particular family dictate their anxiety-specific parent-training approaches ben-
necessity. For example, the therapist might illus- efit youth with anxiety disorders. One study
trate how a parent’s anxious or avoidant behavior investigated the effectiveness of the Positive
may be modeling anxiety. In more severe cases, Parenting Program (Triple P) with anxious youth
referral for outside treatment for the parent may (Özyurt et al., 2019). This study reported signifi-
be warranted. For example, parents suffering cant improvement in child anxiety symptoms,
from PTSD are unlikely to be able to assist their functional impairments, and a decrease in the
child prior to resolving their own symptoms severity of symptoms when compared with wait-
(Carr, 2004). Similarly, families marred by sig- listed youth. Cobham et al. (2017) adapted Triple
nificant conflict may require additional interven- P for youth with anxiety disorders, called Fear-
tion to facilitate their ability to combat anxiety. less Triple P. In a randomized waitlist compari-
Targets of training include improving parent– son trial of 61 participants ages 7–14, 38.7% of
child communication, teaching problem-solving youth in the Fear-less Triple P condition were
skills, increasing positive parental attention, and free from any anxiety diagnosis at the end of
decreasing blame/conflict. These family thera- treatment, compared to 3.4% of youth on the
peutic modules can be added into the anxiety waitlist (Cobham et al., 2017). Parent–Child
treatment sessions seamlessly (e.g., Wood et al., Interaction Therapy (PCIT) was also adapted for
2006). However, long-standing psychiatric ill- treatment of anxious youth. The CALM
ness in children, parents, or both may necessitate (Coaching Approach behavior and Leading by
more intensive prerequisite or concurrent family Modeling) Program was adapted from standard
therapy. If family therapy cannot be imple- PCIT to treat anxiety disorders in youth ages 3–7
mented (with an extremely caustic family), e.g., (Comer et al., 2018). Results from a pilot trial of
because a parent refuses to participate or all the 10 youth suggest that the CALM Program is a
blame is placed on the child, then this is one of feasible treatment for childhood anxiety (Comer
the few situations that individual child therapy et al., 2012). In addition, the CALM Program has
with minimal parent involvement may be been adapted for remote delivery, referred to as
warranted. the iCALM Telehealth Program (Comer et al.,
416
Table 28.1 Select controlled parent-training trials for child anxiety

Study Diagnoses N Ages Sessions Conditions Parent contenta Outcome
Barrett et al. (1996) GAD, SOP 70 7–14 12 Parent and child CBT 1, 2, 3, 4, 6 Parent + Child = Child only
together; child-only CBT; WL > WL*
Barrett (1998) GAD, SOP 60 7–14 12, Group Group child-only CBT; group 1, 2, 3, 4, 6 Parent + Child > Child only
parent and child CBT > WL**; Parent + Child =
together; WL Child only > WL*
Cartwright-Hatton N/A 74 2.7–9 10, Group Group parent training (without Parent training > WL*
et al. (2011) child); WL
Cobham et al. (2017) GAD, SOP, SP, 61 7–14 6, Group Group parent training (without 1, 2, 3, 4, 5 Parent training > WL*
SAD, OCD child); WL
Comer et al. (2021) SOP, GAD, SAD, 40 3–8.9 12 Parent training (with child); 1, 2, 5 Parent training > WL**
SP, OCD WL
Kendall et al. (2008) GAD, SOP; SAD 161 7–14 16 Child-only CBT; parent and 1, 2, 3, 4, 5 Child only = Parent + Child
child CBT together; family > Family education*
education (control)
Lebowitz et al. (2020) GAD, SP, SOP, 124 7–14 12 Parent training (without child); 1, 2, 3, 4, 5, 6 Parent training = Child-only
SAD child-only CBT CBT**
Nauta et al. (2003) GAD, SP, SOP, 79 7–18 12 Child-only CBT; child-only 1, 2, 3 Child-only CBT = Child +
SAD, PD CBT + 7 sessions of parent parent training > WL
training (without child); WL
Özyurt et al. (2019) GAD, SP, SOP, 74 8–12 8, Group Group parent training (without 1, 2, 3, 4, 5 Parent training > WL***
SAD child); WL
Wood et al. (2006) OCD, GAD, SP, 40 6–13 12–16 Child-only CBT; parent and 1, 2, 3, 4, 5 Parent + Child > Child only
SOP, SAD child CBT together **
Selected studies must have (1) with/without parent comparison conditions, (2) controlled design, and (3) outcome based on diagnostic status or clinician rating of improvement
or clinical symptoms using a well-standardized instrument
Abbreviations: GAD generalized anxiety disorder (or overanxious disorder, DSM-III-R), SP specific phobia/simple phobia, SOP social phobia/social anxiety disorder, SAD sepa-
ration anxiety disorder, OCD obsessive-compulsive disorder, PTSD posttraumatic stress disorder, CBT cognitive-behavioral therapy, WL wait list
* = Outcome based on no longer meeting diagnostic criteria; ** = outcome based on clinician ratings of improvement; *** = outcome based on clinician-rated symptom decrease
for targeted disorder (e.g., PTSD symptoms)
Parent treatment components: 1 = psychoeducation; 2 = contingency management; 3 = parent anxiety management; 4 = parent–child problem-solving/communication training;
5 = in-session training for parents to deliver CBT components; 6 = parents trained to model of coping behaviors
a
Based on review of the study and reviews by Ginsburg and Schlossberg (2002) and Silverman et al. (2008)
A. B. Lewin and K. Kudryk
2021). A randomized controlled trial with 40 lack of change in diagnostic status and/or lack of
youth ages 3–8.9 found that 60% of children who clinician-rated symptom improvement) to struc-
participated in iCALM were classified as tured parent training or family therapeutic
responders by the 6-month follow-up (Comer components.
et al., 2021). In addition, there were significantly Despite these results, expert guidelines and
greater reductions in child anxiety symptoms, consensus support parent inclusion in the treat-
fear, discomfort, and anxiety-related social ment of child anxiety (American Academy of
impairment compared to those on the waitlist. Child and Adolescent Psychiatry [AACAP],
Parent-based interventions, specifically for the 2007; AACAP, 1998; Cartwright-Hatton et al.,
treatment of childhood anxiety disorders, have 2004; Ginsburg & Schlossberg, 2002). Individual
also been developed and tested. One such inter- child CBT, medication, and their combination are
vention is the SPACE (Supportive Parenting for evidence-based interventions (Walkup et al.,
Anxious Childhood Emotions) program 2008). However, the fact that youth-centered
(Lebowitz et al., 2014). In a randomized con- treatments for anxiety have produced reliably
trolled trial of 124 youth ages 7–14 comparing strong outcomes does not negate the possibility
SPACE to CBT, it was found that SPACE is as that resulting changes in the child’s symptoms/
efficacious as CBT (Lebowitz et al., 2020). In behavior impact the family system, possibly pro-
addition, parent ratings of family accommoda- ducing reciprocal family/parenting changes.
tion from those who participated in SPACE were Consequently, the efficacy of individual child
significantly more reduced than CBT (Lebowitz treatments does not supersede potential advan-
et al., 2020). Another anxiety-specific parent- tages for parental inclusion.
based program is Timid to Tiger, a group parent- Although few parenting interventions meet
only CBT-based intervention (Cartwright-Hatton criteria for empirically supported treatments
et al., 2011). In a randomized controlled trial of (Chambless & Hollon, 1998; Nathan & Gorman,
74 youth ages 2.7–9 comparing Timid to Tiger to 2002; Silverman et al., 2008), this is due to meth-
a waitlist, it was found that 57% of youth were odological and procedural variance rather than
free from their primary diagnosis by end of treat- lack of efficacy. Many approaches have not been
ment, compared with 15% of youth on the wait- fairly tested and external validity of the findings
list (Cartwright-Hatton et al., 2011). is mostly absent (Weisz et al., 2005). For exam-
ple, to be considered empirically supported,
interventions must be reproduced using con-
Interpretation and Limitations trolled designs (Chambless & Ollendick, 2001) –
of Research Findings comparing parenting interventions across studies
is like comparing oranges to eggplant. Three dif-
There is a consensus that parents impact the ferent research teams may implement similar
development and maintenance of childhood anxi- interventions, but with slightly different manuals
ety. Additionally, most experts agree that parent and approaches. Even the definition and applica-
involvement is an important aspect of treatment. tion of “parent involvement” or “parent training”
However, the extant research has produced mixed or “family therapy” in the treatment is highly
findings regarding the necessity of parenting variable and inconsistently applied. Whereas
interventions for child anxiety disorders. Across some studies include only single parent-training
studies and specific syndromes, parent-training aspects (e.g., contingency management or psy-
approaches have proved superior to control con- choeducation), other studies are more compre-
ditions (e.g., waitlist/no-treatment controls, hensive. Across studies, the content covered in
active psychosocial controls) and, at the very parent sessions varies, e.g., parental anxiety man-
least, equivocal to child-focused treatment with- agement, family problem-solving, the training of
out substantial parent involvement. Notably, sev- parents to be lay-therapists, and improving par-
eral studies suggest no added benefit (defined by ent–child communication. Nevertheless, the
c onditions may be labeled identically (e.g., fam- vary across studies (e.g., symptom improvement
ily CBT or parent training; see Silverman et al., of rating scales, diagnostic remission, clinician-
2008 for review). Therapist–parent contact rated improvement scales). Additionally, diag-
ranges from brief, post-session “check-ins” to nostic remission may not be sufficiently sensitive
participation in the entire session. In some trials, to treatment effects (especially in comparing two
there are consistent, individual parent-training active treatments; e.g., child-only vs. child + par-
sessions while in others, parents and children are ent components), and many of the best designed
seen concurrently. randomized controlled trials are opting to use
Moreover, results from treatment comparison clinician-rated improvement as an alternative
trials must be interpreted in the context of their (Lewin et al., 2012). Further, raters of improve-
methodological limitations. For example, most of ment and diagnostic status vary across studies –
the aforementioned research involves partici- e.g., child, parent, therapist vs.
pants recruited to university-based study centers independent-observer. Independent evaluators
(Bögels & Siqueland, 2006). Subjects may not be range from undergraduate students to senior psy-
representative of family dysfunction and psycho- chologists and physicians, limiting generaliza-
pathology found in referred or community sam- tion across studies. Moreover, given that
ples (Weisz et al., 1992). Additionally, parenting outcomes are based on parent report (e.g., via a
interventions were not tailored to specific family diagnostic interview), the level of parental par-
needs (Manassis et al., 2002). To maximize ticipation in treatment may influence ratings
adherence and treatment success with cognitive- (Hawley & Weisz, 2005). Comparing group-
behavioral-based therapies for child anxiety, the based treatment to individual family treatments
approaches should be flexible and consider indi- adds to the obfuscation.
vidual family factors and psychosocial stressors On a related note, few studies consider family-
(Albano & Kendall, 2002). It is noteworthy that based improvement outcomes while evaluating
extant research lacks controlled comparisons of merits of parenting and family-based treatment
child-focused vs. child + parent-focused inter- approaches for child anxiety. Child anxiety
ventions targeting participants, specifically iden- occurs within a family system. Although many of
tified on the basis of having family functioning the parent-focused approaches in this chapter
struggles. Given that parent anxiety management describe their interventions as family therapy,
benefited child outcomes for youth of anxious many of the interventions more accurately depict
parents (but not of non-anxious parents; Cobham child-focused procedures with or without some
et al., 1998), targeted approaches appear degree of family (or more frequently parental)
warranted. involvement. In a strict sense, family therapy tar-
Dismantling studies is challenging due to sev- gets the family system and, depending on the
eral other limitations. Study designs run the gam- family theoretical approach, family members are
bit from single subject to randomized controlled seen together, often including multiple parents,
trials (RCTs). Additionally, certain studies exam- siblings, and extended family. The child’s anxiety
ine a broad range of anxiety disorders while oth- is not the focus of the intervention – the family
ers focus on a specific syndrome. Other sample system that produces symptoms (e.g., child anxi-
characteristics limit interpretation: many of the ety) is the target. Comprehensive family-based
extant studies do not include older adolescents or interventions (e.g., Bögels & Siqueland, 2006;
children under age 7, limiting generalizability Wood et al., 2006) suggest that family therapy
(Bögels & Siqueland, 2006). Parent-focused may be superior to individual therapy.
approaches appear promising for young children However, in many cases, comprehensive fam-
(e.g., under age 7) with anxiety (Freeman et al., ily therapy may be an elephant-gun approach to
2014; Johnco et al., 2015; Lewin et al., 2014; treating a child’s anxious symptoms. Although
Rudy et al., 2017) although we lack designs com- many parents readily endorse that parenting and
paring methodologies. Criteria for outcome also other family factors may have impacted their
child’s anxiety, others are steadfast in the “fix- Conclusions and Directions
him” approach and are reluctant to accept parent- for Research and Practice
training, let alone a family-model of treatment. In
fact, parents and children often disagree as to the Although the degree to which parent-training
presenting problem (Hawley & Weisz, 2003). interventions augment benefits from child-
Level of family conflict, communication, accom- focused CBT for child anxiety is unclear, it is the
modation, parent anxiety, and parent psychologi- consensus that family involvement in treatment is
cal awareness might dictate the battery, order, necessary (AACAP, 2007). Although findings are
and extensiveness of family interventional mixed, data suggest that parent- and family-based
techniques. interventions are at least equivalent, if not supe-
Simply increasing parental inclusion within rior, to child-focused interventions. Overall, the
child sessions may increase therapeutic alliance extant literature is limited by significant method-
(Hawley & Weisz, 2005) and consequently ological variability and may underestimate the
improve treatment outcomes. Although parent impact of parent components in the treatment of
contact alone (e.g., education alone; Kendall child anxiety.
et al., 2008) is unlikely to be sufficient for treat- Several research questions remain. First, we
ing anxiety, future studies should compare lack sufficient analysis of specific parenting and
degrees of participation (e.g., parents partici- family behaviors that should be considered when
pate in most/all of every session; parents partici- deciding the optimal level of family involvement
pate in portions of session; separate parent or in a child’s treatment. Second (and relatedly),
family sessions). Exposure and response pre- future research should evaluate targeted
vention (ERP) is critical for anxiety reduction in approaches for specific family problems. In other
youth (Peris et al., 2015). Consequently, parent words, clinicians need tools to identify which
training in ERP is likely the most critical ele- families may benefit from which interventions.
ment for optimizing outcomes, especially with Third, family-based outcomes should be consid-
younger children. There are well over 500 psy- ered. When evaluating the efficacy of parenting
chotherapies for youth mental health (Kazdin, and family interventions, diagnostic status may
2000; Wittenberg, 2006), with over 400 ran- be an insufficient barometer. Finally, research
domized psychotherapy trials (Chorpita et al., should be expanded into community-based sam-
2011). Nevertheless, dissemination and expan- ples, generalizing findings outside of recruited
sion into community settings has not kept pace and relatively homogenous samples.
with development and testing. A focus on dis- There are several considerations when inte-
seminating techniques to parents in community grating parent training and family approaches
settings, based on aggregate findings, could into practice. The first series of recommendations
limit the resource bottleneck and reduce barriers focus on assessment. At the onset of treatment,
related to cost/time. Rather than focusing on the clinician should assess child and parent atti-
specific treatments or programs, teaching par- tudes, attributions, and goals for therapy.
ents how to utilize ERP-based tools should be Additionally, careful screening for significant
prioritized. Models may include education and parental anxiety and family conflict should be
brief support for high-risk families: prevention/ conducted. Throughout treatment, the therapist
managing early onset of symptoms with more should monitor for accommodation, modeling,
substantial support from clinicians for pediatric overprotective behavior, and reinforcement of
cases meeting diagnostic threshold/not respon- anxiety-maintaining behaviors. The second set of
sive to briefer/lower intensity approaches. The considerations includes specific aspects of ther-
family is clearly the agent-for-change in youth apy. First, whenever possible, it might be helpful
anxiety – implementation science-based to meet with the family together. Qualitatively,
research appears the next logical step given a greater in-session parent participation appears to
plethora of RCTs. have advantages (Hawley & Weisz, 2005).
Second, several parent-focused techniques ner report of perceived parental rearing behaviors
and anxiety in children and parents. Personality and
appear helpful, e.g., psychoeducation, training/ Individual Differences, 37(8), 1583–1596. https://doi.
modeling of therapeutic techniques, and contin- org/10.1016/j.paid.2004.02.014
gency management training. Anxiety manage- Bögels, S. M., & Siqueland, L. (2006). Family cogni-
ment for parents and communication skills tive behavioral therapy for children and adoles-
cents with clinical anxiety disorders. Journal of the
training may benefit particular families. American Academy of Child & Adolescent Psychiatry,
Additional family-based interventions (or indi- 45(2), 134–141. https://doi.org/10.1097/01.
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School-Based Interventions
for Child and Adolescent Anxiety 29
Jeremy K. Fox, Samantha Coyle, Taylor Walls,
Avi Kalver, Marcus Flax, Aleta Angelosante,
and Carrie Masia Warner
Anxiety disorders are the most common mental based services. Primary care providers can facili-
health problem among young people, with a life- tate children’s access to mental health services
time prevalence rate of 32% prior to age 18 years but often have difficulty identifying anxiety
(Merikangas et al., 2010). Left untreated, child- (Aydin et al., 2020), can feel ill-equipped to man-
hood anxiety is associated with academic and age and support child anxiety (O’Brien et al.,
social impairment (Swan & Kendall, 2016), a 2017), and are less likely to refer anxious youth
chronic course into adulthood (Costello et al., to mental health services than youth with exter-
2005), and significant costs to families and com- nalizing problems (Wren et al., 2005). Similarly,
munities (Bodden et al., 2008; Pella et al., 2020). students identified as anxious through school-
Yet, despite the clear importance of early and wide screenings are less likely than students with
effective intervention for anxious youth, many other mental health problems to receive follow-
remain unidentified, and more than 80% do not up care from a provider (Husky et al., 2011).
receive treatment (Merikangas et al., 2011). Even Logistical barriers, including long wait-lists and
when anxious youth connect with various health high costs, can also prevent families from access-
service sectors, such as pediatrics and school ing community mental health care. This failure to
mental health, they may not receive evidence- deliver adequate care, combined with the high
rates, impairments, and costs of child and adoles-
J. K. Fox (*) · S. Coyle · T. Walls · A. Kalver · cent anxiety, underscores the critical need for
M. Flax alternate methods of providing anxious youth
Psychology Department, Montclair State University, with effective services.
Montclair, NJ, USA
e-mail: foxjer@montclair.edu
A. Angelosante
Department of Child and Adolescent Psychiatry, New Rationale for School-Based
York University Langone Health, New York, NY, Interventions
USA
C. M. Warner Schools can play an important role in addressing
Psychology Department, Montclair State University, the unmet mental health needs of anxious youth
Montclair, NJ, USA by potentially increasing access to cost-effective
Department of Child and Adolescent Psychiatry, New services. Implementing evidence-based interven-
York University Langone Health, New York, NY, tions in school settings offers a number of advan-
USA
tages over traditional mental health services.
Nathan S. Kline Institute for Psychiatric Research, Because schools provide unparalleled access to
Orangeburg, NY, USA
https://doi.org/10.1007/978-3-031-14080-8_29
426 J. K. Fox et al.
youth, school-based services can reduce logisti- portability of CBT interventions in schools. In
cal barriers, such as cost and transportation contrast to more controlled efficacy research,
(Husky et al., 2011). Training school personnel to these studies examined whether researchers
identify anxiety and implement school-wide could implement these interventions feasibly and
screenings may also facilitate early detection and effectively in the real-world conditions of school
intervention efforts (Fox et al., 2008). In addition, settings and with more open inclusion criteria for
as stigma is among the largest barriers to mental participants. More recently, a growing area of
health care, youth and families might be more research has investigated the dissemination of
accepting of mental health services if offered school-based anxiety interventions. These stud-
among the many routine services provided by ies aim to evaluate whether these interventions
schools (Bowers et al., 2013). can be delivered successfully by school person-
Moreover, the school environment is an eco- nel, including school-based clinicians (e.g.,
logically valid setting to implement evidence- school psychologists) and less-specialized school
based interventions for child and adolescent professionals (e.g., teachers) with limited back-
anxiety. Many common triggers of anxiety occur ground in CBT. These studies are also critical for
at school, such as giving presentations, approach- understanding factors such as training and super-
ing peers, being assertive, using public bath- vision models, which may influence whether
rooms, separating from caregivers, taking exams, schools are able to sustain these interventions
and worrying excessively about grades. As a without significant researcher involvement.
result, school-based anxiety interventions allow This chapter will present four school-based
students to practice new skills and engage in intervention programs for child and adolescent
exposure exercises in everyday situations, anxiety. While there are other school-based anxi-
thereby increasing the likelihood of generaliza- ety interventions in the literature, these four pro-
tion. For instance, children can complete expo- grams were selected because their feasibility and
sures in which they read in front of the class or transportability have been demonstrated in mul-
initiate conversations with peers at a school club. tiple randomized controlled trials, and there have
Peers and teachers can also be enlisted to assist in been significant efforts to investigate whether
exposure tasks (e.g., requesting a peer to start a they can be delivered effectively by school per-
conversation with the anxious student to ensure sonnel. Following the overview of these pro-
repeated practice), and school-based clinicians grams, various issues, challenges, and future
can join students to provide additional coaching directions related to the implementation of
and encouragement (Ryan et al., 2012). In this school-based anxiety interventions will be
way, interventions delivered in school can reduce discussed.
the divide between the clinical setting and the
“real world.”
FRIENDS
School-Based Intervention Program Description

Outcome Research
The FRIENDS program is a school-based univer-
Building on research that established the efficacy sal anxiety prevention program for school-aged
of cognitive-behavioral therapy (CBT) for child youth (Barrett & Turner, 2001), adapted from the
and adolescent anxiety in clinic and laboratory Coping Koala (Barrett et al., 1996), which was
settings (e.g., Cartwright-Hatton et al., 2004; based on the Coping Cat, a cognitive-behavioral
Higa-McMillan et al., 2016), the past 15–20 years treatment for child anxiety (Kendall, 1994).
have witnessed a substantial increase in studies FRIENDS is an acronym designed to help chil-
of anxiety interventions in school settings. These dren remember the skills learned during the pro-
studies initially focused on exploring the trans- gram, which include emotion recognition and
29 School-Based Interventions for Child and Adolescent Anxiety 427
regulation, relaxation skills, cognitive awareness (2001) compared FRIENDS (N = 392), delivered
and restructuring, problem-solving, and in vivo by trained classroom teachers, to a waiting list
exposure. The acronym is as follows: F = Feeling control (N = 139) in seven schools. Self-reported
worried; R = Relax and feel good; I = Inner anxiety significantly decreased from pre- to post-
thoughts; E = Explore plans of action; N = Nice intervention in both conditions, but the magni-
work, reward yourself; D = Don’t forget to tude of change was significantly greater for
practice; S = Stay cool. FRIENDS consists of 10 students who participated in FRIENDS. In addi-
weekly group sessions open to all children, with tion, of those who were classified as “at-risk” for
two booster sessions occurring 1 month and an anxiety disorder based on high-baseline anxi-
3 months after the final group. In addition, four ety ratings, only 25% of those in the FRIENDS
parent sessions are used to inform parents about condition remained at risk at posttreatment com-
the program skills and enhance parenting related pared to 55% of the control group.
to anxiety management. Consistent with these findings, Lock and
Since the initial development of FRIENDS in Barrett (2003) found that, among 336 sixth (ages
2001, a set of FRIENDS programs (Fun 9–10) and ninth graders (ages 14–16) from seven
FRIENDS, FRIENDS for Life, My FRIENDS schools in Australia, students who received
Youth and Adult Resilience) have been devel- FRIENDS, delivered by psychologists and doc-
oped to target various age groups. For example, toral students, reported greater decreases of anxi-
the FRIENDS for Life program targets children ety than those in the control group, a monitoring
ages 7–11 (Barrett, 2012a), whereas the My condition. Moreover, sixth graders reported
FRIENDS Youth program is intended for adoles- greater reductions than ninth graders, suggesting
cents ages 12–16 (Barrett, 2012b). The different that late childhood may be an optimal period to
FRIENDS programs overlap in content but differ deliver FRIENDS. As suggested by the authors,
in their use of developmentally appropriate meth- adolescents may be more likely to have coping
ods for delivering the intervention skills. strategies sufficient for managing anxiety and,
Specifically, while programs for younger chil- thus, benefit less from a prevention program.
dren (e.g., Fun FRIENDS) focus more on play- While limited to child self-report data, all three
based techniques, including puppets, stories, and of these studies showed early promise for the
coloring activities, My FRIENDS Youth utilizes effectiveness of FRIENDS as a universal school-
role-plays, group discussions, and written based prevention program for anxiety.
activities. Subsequent follow-up studies provided evi-
dence for the long-term efficacy of FRIENDS in
preventing and reducing anxiety in children and
Outcome Studies adolescents. For example, in a follow-up evalua-
tion of the aforementioned study by Lowry-
Two early studies (Barrett & Turner, 2001; Webster and colleagues, differences in
Lowry-Webster et al., 2001) offered an initial child-reported anxiety were maintained 1 year
evaluation of FRIENDS as a universal program in following intervention, and 85% of treated youth
10–13-year-olds in Brisbane, Australia. First, who had scored in the clinically elevated range
Barrett and Turner (2001) compared FRIENDS to on baseline anxiety or depression self-report
usual instruction across ten schools randomly measures were diagnosis-free at follow-up, com-
assigned to one of the three conditions: teacher- pared to only 31% of the waiting list group
led intervention (TI; N = 253), psychologist-led (Lowry-Webster et al., 2003). In addition, a fol-
intervention (PI; N = 152), or usual instruction low-up of the aforementioned study by Lock and
(UI; N = 84). Children in both intervention condi- Barrett (2003) indicated that anxiety reductions
tions, compared to children receiving UI, reported associated with FRIENDS were largely main-
significantly decreased anxiety at post-tained at 24 and 36 months post-intervention
intervention. Second, Lowry-Webster et al. (Barrett et al., 2006). At 36 months post-
intervention, only 12% of the FRIENDS group Ahlen et al. (2018) did find an enhanced effect of
was deemed at “high risk” for anxiety disorder the intervention in children with elevated depres-
(i.e., scoring in the top 10% on an anxiety self- sive symptoms at baseline, suggesting the inter-
report measure), compared with 31% of the con- vention could be meaningful for students most at
trol group. Moreover, the age difference from the risk.
initial study persisted at these two follow-up time Of note, Maaloof et al. (2020) recently con-
points, again suggesting that FRIENDS may be ducted a school-based randomized controlled
more beneficial for elementary school-age chil- trial (RCT) that compared the My FRIENDS
dren compared to adolescents. Youth program to a waiting list control group in
280 middle school students (ages 11–13) from
ten schools in Beirut, Lebanon. The program was
Cultural Adaptations translated into Arabic, and the intervention work-
book was adapted to incorporate more locally
In the 20 years since these initial studies in salient examples (e.g., surfing changed to playing
Australia, researchers have evaluated the basketball) and replace English names and role
FRIENDS programs all over the world, from models with more culturally relevant and familiar
schools in high-income countries, such as Great Arabic names. Results showed that students in
Britain (Stallard et al., 2007), Slovenia (Kozina, the My FRIENDS Youth program reported greater
2021), Sweden (Ahlen et al., 2012), and Japan decreases in general emotional and depressive
(Kato & Shimizu, 2017; Matsumoto & Shimizu, symptoms, compared to the control group. In
2016), to low- and middle-income countries, addition, girls in the intervention group reported
such as Brazil (Rivero et al., 2020), Mexico greater reductions in anxiety symptoms, a gender
(Gallegos et al., 2012), Iran (Moharreri & difference that is consistent with previous
Heydari Yazdi, 2017), and Lebanon (Maalouf research showing that girls tend to respond better
et al., 2020). To date, findings have been some- to FRIENDS (Barrett et al., 2006).
what mixed. For instance, in an open trial of FRIENDS has also been adapted to increase
FRIENDS delivered by school nurses in Great its reach to children from low socioeconomic
Britain, featuring 106 children between ages 9 backgrounds. For example, Iizuka et al. (2015)
and 10, decreases in self-reported anxiety and adapted FRIENDS for ethnic minority and low
self-esteem were observed from pre- to post- socioeconomic status students in Australia by
intervention (Stallard et al., 2007) and were substituting creative tasks, music, and art activi-
maintained 12 months later (Stallard et al., 2008). ties for those requiring reading and writing.
In contrast, a trial of the Fun FRIENDS program Results showed that the adapted intervention
delivered by school nurses in Japan (Kato & benefited participants who were at risk for mental
Shimizu, 2017), with 74 children ages 8–9, found health problems at baseline, with 30% of the stu-
that parents of children receiving FRIENDS dents being no longer at risk after the interven-
reported a modest decrease in child anxiety com- tion. Importantly, most students rated the
pared to those in the control group, whereas no culturally adapted intervention as being highly
differences were observed in child-reported anxi- acceptable and useful. Similarly, Eiraldi et al.
ety or depressive symptoms. Similarly, Ahlen (2016) adapted FRIENDS to make it more feasi-
et al. (2018) found no effectiveness of FRIENDS ble for implementation with low-income children
for Life, as led by teachers and culturally adapted from urban schools in the United States. In creat-
for a sample of 695 children (ages 8–11) recruited ing their CBT for Anxiety Treatment in Schools
from 17 schools in Sweden. Although self- program, or CATS, changes were made to the lan-
reported and parent-reported anxiety and depres- guage, cultural fit, methods, number of sessions,
sive symptoms did not change overall from and activities in the intervention manual.
pre- to post-intervention, nor 3 years after the Although findings have yet to be published, the
completion of the program (Ahlen et al., 2019), authors expect that this adaptation will result in a
more engaging and culturally sensitive protocol, parents strategies to encourage their children to
while still maintaining the essential ingredients face their fears, and/or instruct parents how to
of cognitive-behavioral interventions for anxiety. manage their own anxiety to be a more effective
coach and better model for their children. In this
study, 61 elementary school children (ages 7–11),
Implementation Strategies with features or diagnoses of separation, general-
ized, or social anxiety disorder and mild to mod-
Studies of FRIENDS have also examined whether erate symptomatology, were randomized to
the program can be delivered successfully by FRIENDS, FRIENDS with enhanced parent
school personnel. However, findings in this area training (both delivered by experienced CBT
have been mixed. For example, while the original therapists), or a no-treatment control. Clinician-,
study by Barrett and Turner (2001) found that child-, and parent-report anxiety measures dem-
FRIENDS was similarly effective at preventing onstrated significant benefits of both active treat-
anxiety regardless of whether it was led by teach- ments compared to the no-treatment control.
ers or psychologists, other studies have found Results were mixed regarding the additional ben-
that FRIENDS was not effective when delivered efits for the inclusion of parent training, and find-
by teachers (Ahlen et al., 2018) or school nurses ings were largely maintained 3, 12, 24, and
(Kato & Shimizu, 2017). In a larger RCT 36 months after intervention (Bernstein et al.,
(N = 1362 students, from 40 schools), Skryabina 2008).
et al. (2016) found that FRIENDS led by health-
care staff external to the school was more effec-
tive in decreasing social anxiety and generalized Summary
anxiety as compared to FRIENDS led by trained
school staff or usual instruction. Taken together, FRIENDS has been shown to be an effective uni-
these findings suggest that we cannot assume versal prevention program in schools in Australia,
anxiety prevention programs such as FRIENDS where it was originally developed. Evidence
will be as effective when delivered by trained appears more mixed when FRIENDS is evaluated
school staff. Further research will be helpful in in other countries and when it is implemented by
identifying factors that may contribute to suc- trained school personnel, such as teachers and
cessful implementation of FRIENDS by school school nurses. FRIENDS may be more effective
personnel. Interestingly, Ahlen et al. (2018) for children most at risk for anxiety disorders and
found that children whose teachers attended a for elementary school children, rather than ado-
larger number of supervision sessions reported lescents. Overall, these studies suggest that
greater decreases of anxiety compared to chil- FRIENDS has the potential to improve access to
dren whose teachers attended fewer sessions and anxiety interventions across different cultures
children in the control group, suggesting that and in low-resource school settings.
supervision might be an important target for
enhancing the ability of school personnel to
deliver FRIENDS effectively. Cool Kids
Program Overview
Parent Training
Unlike FRIENDS, which is an adaptation of a
Bernstein et al. (2005) evaluated a modified ver- treatment protocol, Cool Kids was designed to be
sion of FRIENDS that incorporated weekly par- an indicated intervention for children and adoles-
ent group training to address the impact of child cents at risk for anxiety disorders (Mifsud &
anxiety on families, help parents understand how Rapee, 2005). Cool Kids consists of eight ses-
family relationships can maintain anxiety, teach sions delivered to small groups of youth during
school hours by a trained mental health provider. Spence Children’s Anxiety Scale (SCAS) or were
Separate child and adolescent protocols are avail- nominated by a teacher, were randomized to
able, and the level of parental involvement varies school-based Cool Kids, home-based Cool Kids,
with the age of participants. More specifically, or a waiting list control group. The school-based
parents may be provided with two information Cool Kids was delivered by school counselors in
sessions to learn about, and engage them in, the a group format, consisting of ten 1-hour sessions
intervention. Weekly content may also be pro- and two parent sessions. The home-based Cool
vided to parents if additional parental involve- Kids was implemented individually with each
ment is needed. Early sessions focus on rationale child by the child’s parent(s), who completed two
for treatment, psychoeducation about anxiety, training sessions. Results showed that children
identifying and restructuring anxious cognitions, who participated in either version of Cool Kids
and promoting emotion identification and regula- experienced greater reductions in child anxiety
tion. By session four, students are encouraged to and anxiety-related interference than the waiting
begin engaging in graded exposures, which are list group, according to parent report but not
emphasized through the remaining sessions, report by children or teachers.
along with skills for problem-solving, social Most recently, Haugland et al. (2020) com-
interaction, handling bullying or teasing, and pared the effectiveness of Cool Kids to a brief
increasing assertiveness. CBT intervention and a waiting list control in a
sample of 313 adolescents, between ages 12 and
16, who had an elevated score on the SCAS. The
Outcome Studies Cool Kids and brief CBT conditions were imple-
mented in a group format by school personnel
To date, Cool Kids has been evaluated in at least (e.g., school nurses) or community mental health
three school-based randomized controlled trials: workers. The Cool Kids intervention consisted of
one comparison with a waiting list control group ten 90-minute sessions, held weekly. The brief
(Mifsud & Rapee, 2005) and two comparisons CBT intervention (Vaag) included five
with attention control groups (Haugland et al., 45–90-minute weekly sessions, with a 5-week
2020; McLoone & Rapee, 2012). Misfud and break between the last two sessions, during which
Rapee (2005) completed the first school-based the students completed exposure tasks with mini-
evaluation of Cool Kids in a sample of 91 chil- mal contact with the group leaders. Findings
dren (ages 8–11) with notable anxiety symptoms showed that students in Cool Kids and Vaag
from nine schools in a low socioeconomic area. reported similar reductions in anxiety symptoms,
Schools were randomly assigned to Cool Kids or depressive symptoms, and anxiety-related
a waiting list control group. Each intervention impairment at post-intervention, and that these
group was implemented by a school counselor in reductions were greater compared to those
conjunction with a community-based mental reported by students in the waiting list condition.
health worker who had attended a 1-day training These decreases were maintained at a 1-year fol-
in the intervention. No ongoing supervision was low-up in both intervention groups.
provided by the trainers. Children who partici-
pated in the active intervention showed signifi-
cant improvement in anxiety symptoms Summary
immediately after intervention and at a 4-month
follow-up, based on child and teacher report. Cool Kids appears to contribute to reductions in
McLoone and Rapee (2012) conducted a anxiety symptoms and anxiety-related impair-
novel investigation of Cool Kids by comparing ment in anxious children and adolescents. These
the implementation of the program in school and findings are largely in line with a meta-analysis
home settings. A total of 152 children (ages conducted by Mychailyszyn (2017), which dem-
7–12), who either had an elevated score on the onstrated the efficacy of Cool Kids as an indi-
cated intervention for anxiety across ing the course of the school day, with sessions
investigations in research, community, school, lasting 40 minutes to coincide with a single class
and other settings. It will be important moving period. The parent sessions address psychoedu-
forward to examine Cool Kids in the context of cation about social anxiety and ways to manage
larger attention control trials and implementation children’s anxiety and facilitate improvement.
solely by school personnel. In addition, given Teacher meetings are designed to educate teach-
findings by Haugland et al. (2020) showing simi- ers about social anxiety, obtain information about
lar outcomes from Cool Kids and a briefer group- which classroom behaviors to target, and enlist
based CBT intervention, further study should their assistance with classroom exposure exer-
explore the utility and effectiveness of potentially cises (e.g., reading aloud, answering questions in
delivering Cool Kids in a briefer, flexible, or class). Finally, the four social events provide real-
modular format. world exposures and opportunities for skills gen-
eralization. Group members practice social
interactions with actual school peers in natural
kills for Academic and Social
S community “hang-outs” (e.g., bowling, school
Success picnic).
Program Overview
Outcome Studies
Skills for Academic and Social Success (SASS;
Masia et al., 1999; Masia Warner et al., 2018) is a SASS has been evaluated in a small open trial
cognitive-behavioral group treatment for social (Masia et al., 2001), a wait-list control trial
anxiety disorder (SAD) in adolescents in the (Masia Warner et al., 2005), an attention control
school setting. SASS is based on Social trial (Masia Warner et al., 2007), and a large
Effectiveness Therapy for Children (SET-C), an effectiveness trial (Masia Warner et al., 2016). In
efficacious, clinic-based treatment for children the wait-list control trial, 35 adolescents with
with SAD that emphasizes exposure, social skills SAD, ages 14–16 years, from two urban paro-
training, and peer generalization exercises chial schools were randomized to either SASS or
(Beidel et al., 2000, 2005). SASS features signifi- a waiting list. Treatment was conducted by a clin-
cant modifications for an adolescent population ical psychologist and a psychology graduate stu-
(e.g., developmentally appropriate social skills, dent trained in the intervention. The SASS
addition of training in realistic thinking) and the intervention was superior to the waiting list in
school environment (e.g., fewer and briefer ses- reducing social anxiety and avoidance and
sions and incorporation of teachers, parents, and enhancing functioning, as noted by blind evalua-
school peers). SASS consists of 12 group school tor, parent, and adolescent ratings. Of the SASS
sessions, two individual meetings, two parent group, 94% were classified as responders, com-
meetings, two teacher meetings, four social pared to only 12% of wait-list participants. In
events attended by group participants and outgo- addition, 67% of SASS participants, versus 6% in
ing school peers, and two booster meetings. The the wait-list group, no longer met diagnostic cri-
12 school sessions include realistic thinking teria for SAD at post-assessment.
(cognitive restructuring), social skills training, The second investigation compared SASS to a
and exposures that are integrated into the school credible attention control in 36 adolescents, ages
environment and include the assistance of school 14–16, with SAD (Masia Warner et al., 2007).
personnel or school peers (e.g., ordering and The attention control omitted therapeutic ele-
returning food in the cafeteria, starting a conver- ments specific to reversing social anxiety but was
sation with a teacher). In addition, two individual matched on other relevant therapy variables. It
meetings focus on setting goals and problem- was designed to match SASS in structure with
solving treatment obstacles. Sessions occur dur- the inclusion of the four social events conducted
without the outgoing school peers. The content outcomes comparable to clinical psychologists
consisted of psychoeducation about social anxi- when provided with training and supervision.
ety, relaxation techniques, and support. At post- These findings point to a model for promoting
treatment, SASS was superior to the attention access to services by preparing frontline school
control in reducing social anxiety and improving professionals to deliver evidence-based care for
overall functioning. Only 7% in the attention underserved youth with SAD, which may extend
control, versus 82% in SASS, were treatment to other anxiety disorders.
responders. In addition, 59% of the SASS group
no longer qualified for a diagnosis of social pho-
bia, versus 0% of the attention control. SASS was School-Based Treatment for Anxiety
also superior to the attention control 6 months Research Study
beyond the cessation of treatment.
To examine whether SASS could be imple- Program Overview
mented effectively by school counselors without
specialized training in CBT, Masia Warner et al. The School-Based Treatment for Anxiety
(2016) conducted an RCT with 138 ninth through Research Study (STARS; Ginsburg et al., 2020),
11th graders from three public high schools. as well as the related Baltimore Child Anxiety
Students were randomized to one of three condi- Treatment Study in the Schools (BCATSS;
tions: SASS as delivered by school counselors Ginsburg et al., 2008, 2012), were conducted to
(C-SASS), SASS as delivered by clinical psychol- evaluate a treatment program for child anxiety
ogists with experience in CBT for youth anxiety disorders that was delivered in school districts by
(P-SASS), and Skills for Living (SFL), a non- school-based clinicians. The BCATSS was ini-
specific, manualized school counseling group pro- tially adapted for, and conducted in, an inner-city
gram. School counselors completed a 5-hour environment that is typically underserved.
training workshop and co-led a 12-week SASS However, the initial evaluation of the CBT treat-
training group with a clinical postdoctoral fellow. ment used in the BCATSS has evolved into a
Following this, school counselors received weekly broader examination of the use of CBT in school-
consultation during independent SASS implemen- based anxiety treatment that can be used in dif-
tation. Both immediately posttreatment and at a ferent socioeconomic school settings. In contrast
5-month follow-up, treatment response was signifi- to most other school interventions, the treatment
cantly greater in C-SASS (65% and 85%) and (henceforth known as the STARS program) is
P-SASS (66% and 72%) than in SFL (18.6% and delivered in an individual rather than group for-
25.6%). In addition, C-SASS and P-SASS partici- mat. STARS consists of 12 sessions conducted
pants had lower severity of SAD at both time points during regular school hours. Sessions are approx-
than students who completed SFL. Diagnostic imately 30–45 minutes in length in order to coin-
remission was also higher for C-SASS (22% and cide with a single class period. The program was
39%) and P-SASS (28% and 28%) than SFL (7% designed for delivery by school counselors, social
and 12%) at posttreatment and follow-up. No dif- workers, and psychologists following a brief
ferences between C-SASS and P-SASS were training on the manual. A unique feature of the
observed on the main clinical outcomes. STARS program is that, while the protocol is
manualized, it employs a modular approach that
allows the therapist to decide which of the core
Summary cognitive-behavioral strategies should be
addressed in any given session. The treatment
Masia Warner and colleagues have demonstrated modules include psychoeducation, contingency
the specific benefits of treating SAD in the school management, relaxation, exposure, cognitive
setting. School counselors were able to imple- restructuring, problem- solving, and relapse
ment the SASS program with positive student prevention.
Outcome Studies with 42% and 37% of students classified as

responders, respectively. No differences were
In a small open pilot study of nine African observed between the conditions when examin-
American adolescents with generalized anxiety ing child-reported anxiety from pretreatment to
disorder (GAD), social anxiety disorder (SAD), posttreatment. However, STARS was shown to be
or specific phobia, Ginsburg and Drake (2002) more effective in reducing parent-reported child
compared their school-based cognitive-anxiety symptoms, as well as for students with a
behavioral treatment to an attention control higher severity of anxiety symptoms (Ginsburg
group. Three out of four treatment completers et al., 2020).
(75%) no longer met criteria for an anxiety disor- Ginsburg and colleagues have also explored
der at the end of treatment, while only one of five the implementation of CBT in schools by school
youth (20%) in the attention control group remit- nurses. Recognizing that children and adoles-
ted to nonclinical status. Results supported the cents with anxiety frequently seek assistance
feasibility and possible benefits of this approach. from their school nurses, Ginsburg and col-
To evaluate the effectiveness of the STARS leagues sought to develop an intervention that
program further, Ginsburg and colleagues con- could increase access to evidence-based care at
ducted two attention-control trials with a larger school and allow school nurses to address factors
number of participants in which they compared contributing to student anxiety. The resulting
STARS to usual care provided by schools. 8-week intervention, the Child Anxiety Learning
Ginsburg et al. (2012) randomly assigned 32 stu- Modules (CALM), focuses on the core compo-
dents (ages 7–17) from the Baltimore City public nents of CBT, such as psychoeducation,
school system to STARS or a treatment as usual cognitive- restructuring, relaxation strategies,
(TAU) group that did not involve CBT strategies. exposure, problem-solving, and relapse preven-
Students were primarily African American, and tion. In order to provide flexibility for nurses and
all had a primary diagnosis of GAD, SAD, sepa- individualized treatment for students, CALM is a
ration anxiety disorder, or specific phobia. A total modular program and does not require a specific
of 11 social workers and counselors were also number of sessions. To date, CALM has been
randomly assigned to serve as an implementer of evaluated in an open trial (Muggeo et al., 2017)
one of the two treatment conditions. Both condi- and an RCT (Ginsburg et al., 2021). The open
tions were associated with reductions of anxiety trial (Muggeo et al., 2017) was composed of 11
symptoms, based on child and parent report, by children with GAD, separation anxiety disorder,
posttreatment and a 1-month follow-up, and no or social phobia. There was a significant decrease
differences were found between the conditions. in child-reported and parent-reported child anxi-
Ginsburg et al. (2020) conducted a random- ety from pre- to posttreatment, with 45% of chil-
ized attention control trial that compared STARS dren no longer meeting criteria for an anxiety
to school-based TAU in 216 children (ages 6–18) disorder. Ginsburg et al. (2021) expanded on this
throughout Connecticut and Maryland, along initial trial by randomly assigning 54 children
with 62 school psychologists and school social with elevated anxiety symptoms to CALM or a
workers. All students had a primary anxiety dis- control condition, CALM-R, which focused on
order diagnosis. The sample was less diverse in relaxation skills. Anxiety symptoms decreased
race/ethnicity, with 62% of the students identified across both groups from pre-intervention to post-
as Caucasian. Independent evaluators who intervention; however, no differences were
observed the TAU condition found that very few observed when comparing CALM and CALM-R.
sessions incorporated CBT skills and that the Looking ahead, Ginsburg and colleagues are
TAU providers were low in competence when in the process of examining whether teachers can
providing CBT skills (Ginsburg et al., 2019a). successfully identify and address problematic
Findings indicated that STARS and TAU were anxiety in their students. Given that anxiety com-
both effective in decreasing anxiety symptoms, monly manifests in the classroom, Ginsburg and
colleagues propose that teachers are well posi- tions when implemented by trained school
tioned for helping students with anxiety and have personnel.
thus developed the Teacher Anxiety Program for
Elementary Students (TAPES), a school-based
CBT intervention delivered to individual families I mplementation Issues and Future
by teachers. Over the course of 8 weeks, teachers Directions
conduct five 30-minute joint meetings with each
student and their parent(s) to deliver each module Based on the promising findings described thus
of TAPES, which include relaxation skills, expo- far, the delivery of evidence-based interventions
sure, and cognitive restructuring. Teachers par- in schools has potential to help remediate the
ticipate in an initial full-day in-person training in high rates of child and adolescent anxiety.
TAPES, as well as receive 30 minutes of weekly Moving forward, several issues and challenges
expert consultation while implementing the inter- will be important to address in order to advance
vention. In an RCT funded by the US Department the implementation of school-based mental
of Education, a racially, ethnically, and socioeco- health services.
nomically diverse sample of 60 elementary
school students with elevated anxiety symptoms,
along with 40 teachers, have been randomly Multi-Tiered Systems of Support
assigned to the TAPES intervention or a control
condition in which teachers attend 3 hours of a Youth who experience anxiety are unfortunately
typical professional development seminar on stu- not always eligible to receive interventions within
dent anxiety. The study is ongoing (see Ginsburg the school context. For instance, even though the
et al., 2019b for additional information). Individuals with Disabilities in Education
Improvement Act (IDEIA, 2004) requires that
students with severe anxiety are evaluated and
Summary provided with an Individualized Education Plan
(IEP), these services are only provided if their
Studies by Ginsburg and colleagues show prom- anxiety significantly affects their educational
ise for increasing accessibility to individual CBT performance. Students who demonstrate signifi-
for anxiety disorders in urban and inner city cant anxiety but not an educational deficit may be
schools through delivery by school personnel. able to receive school-based accommodations
However, their CBT programs yielded similar and supports as part of a 504 plan (Conroy et al.,
outcomes to TAU (Ginsburg et al., 2012, 2020) 2021). However, IEP and 504 plans can be chal-
and a relaxation-based program (Ginsburg et al., lenging for families to obtain and available only
2021). School personnel may have found it chal- to students with severe anxiety (August et al.,
lenging to deliver a modular individual treatment 2018). In addition, while IEPs and 504 plans
for multiple anxiety disorders. In contrast, a sys- offer supports, many of these supports for anxiety
tematic manualized group treatment for a single are not evidence-based and often include accom-
disorder, such as the SASS treatment for SAD modations that do not address the root of the
described previously, may be easier for school problem (e.g., exposure to anxiety-provoking
personnel to learn and implement with skill and situations) but instead inadvertently maintain stu-
fidelity. In addition, group treatments, which dent anxiety (e.g., accommodations that allow for
allow students to engage in social skills and continued avoidance of anxiety-provoking situa-
exposure exercises with their peers, might be tions; Conroy et al., 2020; Harrison et al., 2013).
more beneficial for students with certain types of For example, one recent survey of school mental
anxiety, such as social anxiety. Future research health professionals found that most respondents
should explore the relative effectiveness and reported using accommodations or supports that
fidelity of individual and group CBT interven- promote avoidance of anxiety-provoking
situations, such as letting youth sit in class but is how to identify youth who require intervention.
not participate (Conroy et al., 2020). As anxiety disorders often go unnoticed and
As concerns have been raised about limited unidentified (Papandrea & Winefield, 2011), it is
access to evidence-based mental health services important that schools utilize a multi-method,
in schools, there has been increasing advocacy comprehensive approach to understand the needs
for schools to move away from a traditional med- of students. A first step in this approach is typi-
ical model of school-based mental health treat- cally to conduct universal screenings for anxiety
ment and toward a preventative model using a and other related problems that involve adminis-
Multi-Tiered Systems of Support (MTSS) frame- tering evidence-based assessment tools to stu-
work. An MTSS framework uses data to make dents, parents, and/or teachers. This universal
informed decisions about students’ levels of screening process allows educators to make data-
functioning and appropriately allocate resources informed decisions about how to effectively allo-
and deliver interventions at varying levels of cate the limited resources available within a
intensity (August et al., 2018). This approach school, select appropriate interventions, and
allows for students who may have significant identify which students would benefit from inter-
anxiety, but do not demonstrate the required edu- ventions (Dowdy et al., 2015; Nickerson, 2019).
cational impact for an IEP or 504 plan, to receive Although universal screenings are commonly
early interventions and supports that can prevent used by targeted prevention programs successful
their anxiety from becoming severe enough to in promoting social and emotional well-being in
cause academic difficulties. MTSS typically youth (Durlak et al., 2011), and may be an afford-
includes three tiers: Tier 1, which involves uni- able option for schools (Simon et al., 2013),
versal prevention for all students; Tier 2, which questions do remain regarding their efficiency
focuses on small group interventions for those at and cost-effectiveness. Future studies should
risk for, or displaying signs of, anxiety; and Tier explore the relative utility and affordability of
3, which consists of individualized treatment for other methods of identifying students, such as
students who do not respond to previous inter- teacher referral, reviewing school records, and
ventions. While the school-based anxiety inter- behavioral observations (Dowdy et al., 2015).
ventions described in this chapter are aligned
with at least one tier, such as FRIENDS (a univer-
sal intervention) and STARS (an individualized Progress Monitoring
treatment), further research is needed to evaluate
a full MTSS three-tiered model for child and ado- In addition to the initial assessment of anxiety to
lescent anxiety in schools. A research methodol- identify those who require additional supports, it
ogy developed by August et al. (2018), Sequential is important that a progress-monitoring proce-
Multiple Assignment Randomized Trials dure be in place to evaluate progress and deter-
(SMART), may be useful in this effort to evaluate mine whether youth may require more intensive
the adaptive intervention strategies at the core of supports if they are not responding to evidence-
the MTSS model. If effective, this model would based interventions provided through their MTSS
allow educators to select, adapt, and implement system (Conroy et al., 2021). One tool that can be
evidence-based interventions that are appropri- helpful to monitor progress is the use of Daily
ately mapped to the needs of anxious students Behavior Report Cards (DBRC), which provide
within a school. clear and explicit goals for students to meet each
day and monitor students’ progress toward those
goals (Riley-Tillman et al., 2008). This can serve
Identification of Anxious Youth as a method to not only measure students’
response to intervention but also provide feed-
One challenge to effectively implementing an back to students on their performance, celebrate
MTSS program for child and adolescent anxiety their successes, and communicate progress to
caregivers to reinforce within the home setting. these interventions effectively. However, school
Other potential methods for monitoring clinically personnel in these studies were provided with
meaningful change may include student and par- training, ongoing supervision, and other support
ent ratings of clinical improvement, though there from researchers. It remains uncertain whether
are concerns of reporting biases, such as social school personnel can continue these services suc-
desirability (Fox et al., 2017). Therefore, further cessfully without researcher involvement and/or
research should investigate strategies that facili- financial support and resources from school lead-
tate honest and accurate reports of progress in the ership. School-based clinicians, such as school
context of school-based anxiety interventions. counselors, school psychologists, and school
social workers, often have highly demanding
caseloads and may lack sufficient time and fund-
School Culture and Climate ing to offer additional mental health services.
Indeed, limited time and financial resources,
Successful entry of novel mental health programs along with the overall shortage of trained mental
into the school system requires an awareness of health professionals within schools, have been
the school climate and the attitudes of key stake- identified by school personnel as among their
holders. Federal and state initiatives have empha- main barriers to implementing mental health
sized the importance of positive and supportive interventions in their schools (Wang et al., 2020).
school climates as a necessary ingredient for In addition, if school staff who provide services
effective schools, and many states have imple- for anxious students are emotionally exhausted by
mented social–emotional learning standards to their work, they may be more likely to utilize non-
ensure that social and emotional skills are priori- evidence-based intervention strategies (Conroy
tized (Zins & Elias, 2007). Despite such initia- et al., 2020). Therefore, further research is needed
tives, school culture and climate can pose to examine the sustainability of anxiety interven-
significant barriers to implementing school-based tion programs delivered by school-based clini-
interventions for anxiety disorders. For example, cians over time without the ongoing involvement
as academic instruction is the primary mission of of researchers.
schools, school administrators and parents may
question the value of programs that do not
directly advance these goals. Therefore, it is Family–School–Community
important that interventions avoid interfering Partnerships
with class instruction. Sessions for group inter-
ventions can be rotated weekly to ensure that stu- Building capacity within the school setting to rec-
dents do not miss the same class repeatedly, and ognize and treat mental health challenges is criti-
conducting interventions individually can pro- cal to ensuring that MTSS programs can be
vide flexibility to schedule sessions during non- effective in supporting anxious youth (Sanchez
academic periods. et al., 2018). Researchers have suggested that one
method to achieve this is for schools to develop
strong family–school–community partnerships.
Service Providers For example, mental health professionals outside
of the school setting can help to support and
Another important consideration in the effective address some of the challenges of implementing
implementation of school-based mental health evidence-based interventions through consulta-
services is identifying a skilled and interested pro- tion with school professionals (Conroy et al.,
vider within the school. As highlighted in this 2021). Given that outside mental health profes-
chapter, an increasing number of school-based sionals have expertise in evidence-based anxiety
anxiety intervention studies have utilized trained interventions, educators have expertise in imple-
school personnel as service providers, with sev- menting school-based services and the educa-
eral showing that school personnel can implement tional setting, and families have expertise on their
children, collaboration among school, family, and with school-based clinicians for components that
community is central to promoting student suc- require support. This would ease the burden on
cess. This consultative framework is in line with school personnel while still ensuring that stu-
the National Association of School Psychologists dents receive adequate intervention. While
professional standards that emphasize family– computer-assisted CBT has been shown to be
school–community partnerships as one of the efficacious in treating youth anxiety in a clinical
main domain areas for professional practice setting (Khanna & Kendall, 2010) and a commu-
(NASP, 2020), and further study is needed to nity setting (Crawford et al., 2013), studies of
explore its utility in the context of school-based online anxiety interventions in school settings,
interventions for child and adolescent anxiety. such as e-Couch (Calear et al., 2016) and Positive
Search Training (Waters et al., 2019), have shown
limited effectiveness thus far.
Cost-Effectiveness In addition to innovative technologies, other
cost-effective strategies for schools, such as brief
Sustaining the delivery of school-based mental and modular interventions, should be explored.
health services for youth anxiety will require such Brief interventions that require less time from
services to be cost-effective for schools. However, school-based clinicians may hold promise, as
the cost-effectiveness of school-based interven- evidenced by an initial trial of the DISCOVER
tions for anxiety remains unclear. To our knowl- program, a 1-day CBT workshop for stress, anxi-
edge, only one published study has examined this ety, and depression that was superior to a waiting
question, finding that the FRIENDS universal pre- list condition in a sample of adolescents from
vention program was not cost-effective when inner-city schools in the United Kingdom (Brown
delivered to elementary school students in et al., 2019). Modular CBT designs, which allow
England (Stallard et al., 2015). Further research is clinicians to select strategies to meet children’s
thus needed to understand the relative cost- individual needs, may also offer a more efficient
effectiveness of different models of intervention, means of treating anxious students than a full
such as a comparison of universal prevention pro- intervention program. Support for this approach
grams with more targeted programs for youth comes from an RCT evaluating a modular ver-
with anxiety risk factors, symptoms, and/or diag- sion of the Building Confidence CBT program in
noses. For instance, universal prevention pro- a sample of children with anxiety disorders from
grams may be more efficient given costs associated two elementary schools in the United States. This
with mental health screening; however, if pro- modular program outperformed a wait-list condi-
grams have better clinical outcomes when provid- tion on treatment response, diagnostic outcomes,
ing services only to youth with anxiety, the and caregiver-reported anxiety after the interven-
benefits of more targeted prevention and treat- tion (Chiu et al., 2013) and 1 year later (Galla
ment programs may outweigh the initial cost of et al., 2012).
detection. Given that youth often experience both anxi-
ety and depression, it may be more efficient to
offer CBT techniques in a transdiagnostic format
Innovative Formats (i.e., targeting both difficulties) as a way to
increase the reach and impact of the intervention.
Further study is also needed to develop and eval- One example of this approach, the Emotion uni-
uate approaches to delivering effective school- versal prevention program, was associated with
based interventions while limiting costs. For greater reductions of anxious and depressive
example, online programs for child and adoles- symptoms compared to usual care in children
cent anxiety could be well suited for the school from schools in Norway (Martinsen et al., 2019),
setting. Students could complete online sessions though some outcomes were not maintained
on their own during the school day and check in 1 year later (Loevaas et al., 2020). Therefore, fur-
ther study is needed to examine the utility and Studies indicate that training frontline school per-
effectiveness of transdiagnostic interventions. sonnel, such as teachers and school counselors, to
deliver cognitive-behavioral anxiety interventions
may be feasible and effective. Several issues and
Diversity and Social Justice challenges related to the implementation of school-
based interventions for child and adolescent anxi-
School-based interventions for anxiety are not a ety will be important to address in the future.
one-size-fits-all approach but must be sensitive to These include the need to explore a Multi-Tiered
the unique characteristics of students within a System of Support involving evidence-based,
school. Despite the high rates of anxiety disor- cost-effective, and adaptive strategies for identify-
ders in students of color, mental health service ing and addressing anxiety in schools, a means of
utilization by this population is especially low fostering family–school–community partnerships,
(Gudiño et al., 2009). The benefits of school- and culturally sensitive services that engage his-
based mental health services have been limited torically marginalized youth. Continued research
by racial and ethnic disparities in access and in these areas will be essential for developing a
enrollment, particularly for internalizing condi- sustainable model for promoting effective care for
tions (Bear et al., 2014; Gudiño et al., 2009). anxiety in school settings.
Additionally, racially and ethnically minoritized
youth may be presented with unique challenges, Author Note This chapter was partially supported by the
such as racism and discrimination, which can Institute of Education Sciences, US Department of
exacerbate anxiety symptoms and place them at Education, through Grant R305A200013 to Dr. Masia
Warner. The opinions expressed are those of the authors
higher risk for negative outcomes (Graham et al., and do not represent views of the institute or the US
2016). The racialized stressors experienced by Department of Education.
Black youth may also create anxiety symptoms
that are not typically included in commonly used
measures of anxiety (Anderson et al., 2019). As a References
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Social Disability and Impairment
in Childhood Anxiety 30
Laura John-Mora, Abigail M. Ross,
and Jordana Muroff
Anxiety disorders cause severe impairment and ment is understood, addressed, and prevented
disability with respect to an individual’s quality where possible.
of life and social functioning, especially when Anxiety is the sixth leading cause of all dis-
untreated (Strawn et al., 2020). Worldwide preva- ability worldwide (Baxter et al., 2014).
lence of any anxiety disorder in children and ado- Impairment among adults with anxiety manifests
lescents is estimated at 6.5% (Polanczyk et al., itself through considerable economic costs
2015). Meanwhile, rates of childhood anxiety related to medical care as well as decreased work
disorders in the United States are estimated to be productivity (Greenberg et al., 1999). In families
between 15% and 20%, representing the most with clinically anxious children, societal costs
prevalent form of psychopathology in children have been estimated to reach 20 times those
and adolescents (Kessler et al., 2012a or b; incurred by families in the general population
Merikangas et al., 2010). Further, the median age (Bodden et al., 2008). Anxiety disorder induced
of onset for anxiety disorders in the United States impairment in children includes difficulty in the
is 6 years, which is significantly earlier than the school environment (Strauss et al., 1989; de
age of onset for other major mental disorders Lijster et al., 2018), problematic social interac-
(Kessler et al., 2005a or b). Impairment that is tions (Essau et al., 2000; Crawford & Manassis,
associated with anxiety is significant. In the 2011), distress in family life (Turner et al., 1987;
National Comorbidity Survey (NCS), approxi- Bernstein et al., 1996; Senaratne et al., 2010),
mately 8.3% of adolescent and 22.8% of adult and can result in the inhibition of the successful
respondents reported severe impairment, sug- completion of discrete developmental and plan-
gesting that impairment worsens over time and ning tasks (Rodrigues et al., 2019).
with age (Harvard Medical School, 2007; Kessler Numerous studies indicate that adolescents
et al., 2005a or b). Given that anxiety is the most with anxiety disorders struggle with loneliness,
prevalent class of disorders (Kessler et al., difficulty in interpersonal relationships, lower
2005a or b), it is critical that the resulting impair- social competence, and feelings of impairment in
school settings (e.g., Asselmann et al., 2017; de
L. John-Mora · A. M. Ross (*) Lijster et al., 2018; Settipani & Kendall, 2012).
Fordham University Graduate School of Social Social problems and peer adversity have also
Service, New York, NY, USA been linked to the development and prolongation
e-mail: aross28@fordham.edu of anxiety (Settipani & Kendall, 2012), suggest-
J. Muroff ing that specific behaviors associated with social
Boston University School of Social Work, Boston, maladjustment in anxious children have an
MA, USA
https://doi.org/10.1007/978-3-031-14080-8_30
446 L. John-Mora et al.
impact on the way they are perceived by peers, interpersonal capacities, including navigation of
leading to lower rates of positive peer responses family, peer, and romantic relationships (Bird
(Gazelle, 2008). et al., 2005; Langley et al., 2014). This chapter
Evidence from a number of studies (e.g., describes both the scope and manifestation of
Mychailyszyn et al., 2010; Owens et al., 2012; anxiety disorder-specific impairment in social
Weems et al., 2013) suggests that anxiety is often functioning in children and adolescents accord-
associated with a range of academic difficulties ing to diagnostic and statistical manual of mental
for school-aged children and youth. In a 2014 disorders, fifth edition (DSM-5) diagnostic cate-
study examining school-specific dimensions of gories and concludes with a discussion of impair-
the Child Anxiety Impact Scale – Parent Version ment related to notable comorbidities,
(CAIS-P; Langley et al., 2004, 2014), Nail et al. subthreshold anxiety problems, developmental
(2014) found that close to 50% of participants stages, measurement, and social context.
had an impairment in four out of seven academic
items (completing assignments, concentrating on
work, doing homework, getting good grades, giv- Disorder-Specific Impairment
ing oral reports, taking tests/exams and writing in
class). The most common impairment reported Separation Anxiety Disorder (SAD)
was difficulty concentrating on schoolwork,
which suggests this is a symptom associated with Separation Anxiety Disorder (SAD) interferes
most anxiety disorders (Nail et al., 2014). with an individual’s ability to cope with separa-
Though the manifestation of anxiety-related tion from home or primary caregivers without
impairment in children differs from that in adults, persistent and excessive worry, distress, and
systematic examinations of this phenomenon are physical symptoms such as nausea, vomiting,
not reported as extensively in the child and ado- stomachaches, headaches, and other physical
lescent literature as in the adult literature (e.g., symptoms (American Psychiatric Association
McKnight et al., 2016). A clear articulation of [APA], 2013). Issues related to attachments dur-
what is meant by “impairment” has yet to be ing childhood can affect an individual’s ability to
established with respect to child anxiety disor- tolerate anxiety, self-soothe, regulate affect, indi-
ders. Standards for judging anxiety as “dysfunc- viduate (Milrod et al., 2014), and ultimately may
tional” in nature vary across environmental lead to an anxious attachment style that may con-
contexts, cultural values, family attitudes, and strain the ability to develop and foster social sup-
developmental stages (Egger & Angold, 2006). ports (Roberson-Nay et al., 2012). SAD is
For example, parents of very young children may associated with disability and significant impair-
not judge avoidance of being alone, a symptom ment in academic, family, and social domains of
of separation anxiety, to be “impairing” behavior. functioning, as well as reduced quality of life
In addition, measures of anxiety-related func- (Aderka et al., 2012).
tional impairment in children are limited and In children and adolescence specifically, SAD
tend to be focused on symptom severity rather prevalence rates range from 3.5% to 6.7%, with a
than domains of disability (Piacentini et al., mean onset age of 8 years (Black, 1995;
2007). Merikangas et al., 2010; Beesdo et al., 2010). In
In this chapter, the concept of impaired func- youth with SAD, full onset of anxiety symptoms
tioning is conceptualized as an absence of nor- generally emerges by age 12, with behavioral
mative adaptation (or poor performance) with inhibition present early in the disorder develop-
respect to (1) school performance (related to ment trajectory (Strawn et al., 2020). Children
work completion, attendance, tardiness, and who exhibit maladaptive functioning and symp-
homework completion), (2) a range of develop- toms of SAD early in development may have dif-
mentally appropriate self-fulfillment activities, ficulty learning the skills needed to cope with
including the ability to care for oneself, and (3) intense emotions and anxiety, which may ulti-
30 Social Disability and Impairment in Childhood Anxiety 447
mately amplify the effect of the disorder across Panic Disorder

the lifespan (Kossowsky et al., 2013).
Evidence of a developmental trajectory from Children and adolescents with PD are likely to
stranger anxiety in infancy to childhood SAD has avoid everyday settings such as school, shopping
begun to emerge (Kossowsky et al., 2013). centers, restaurants, elevators, and parks due to
Maladaptive functioning early in life may impede excessive fear of future panic attacks (Elkins
development of coping skills for anxiety and et al., 2014). Panic attacks are associated with a
other strong emotions, creating a setback in number of problems, the most frequent being
healthy development and potentially leading to avoiding social situations due to anticipatory fear
prolonged impairment and disorder. A growing of another attack and intensely unpleasant physi-
body of research suggests that childhood SAD ological symptoms such as chest pains, palpita-
can function as a precursor to mental and physi- tions, trembling, nausea, and chills/hot flashes
cal health problems, persistent distress in social (Essau et al., 2000; Elkins et al., 2014). The acute
settings, ongoing somatic symptoms, and aca- physical symptoms that accompany panic attacks
demic issues (Battaglia, 2015). While SAD is (e.g., nausea, chest pains, heart palpitations, etc.)
associated with increased risk of secondary anxi- can create additional distress, which may increase
ety and mood disorders (Milrod et al., 2014), the future impairment.
association between childhood SAD and panic Though PD is less prevalent compared to
disorder (PD) is particularly significant (Battaglia, other psychiatric disorders in the general popula-
2015). Results from a meta-analysis of 20 epide- tion, between 12% and 25% of the general popu-
miological studies indicate that children with lation suffers from a panic attack at least once in
SAD are nearly 3.5 times more likely to develop their lifetime (de Jonge et al., 2016; Grant et al.,
PD later in life (Kossowsky et al., 2013), suggest- 2006; Kessler et al., 2006), with nearly two-thirds
ing that a diagnosis of SAD may in fact be indica- experiencing recurrent attacks (de Jonge et al.,
tive of early onset PD in youth (Doerfler et al., 2016). The 12-month prevalence among adults
2008; Roberson-Nay et al., 2012). and adolescents in the United States is between
SAD has also been shown to be associated 2% and 3%, with a median age of onset of
with impaired academic performance (Battaglia 20–24 years (Kessler et al., 2005a or b,
et al., 2017) and increased rates of suicidal ide- 2012a or b). Onset of PD in childhood and ado-
ation (Pini et al., 2021). School refusal has been lescence is associated with other comorbid anxi-
reported in approximately 75% of children with ety disorders, depression, and suicidal ideation
SAD (Masi et al., 2001), yet may be more preva- and attempts (Beesdo et al., 2009; Masi et al.,
lent in youth with comorbid SAD and 2000a or b; Elkins et al., 2014), with earlier onset
PD. Findings from a study comparing a sample of the disorder associated with a more severe
of youth with SAD only (n = 63) to counterparts impairment and chronic progression of symp-
with comorbid SAD and PD (n = 31) revealed a toms across the lifespan (Merikangas et al., 2010;
later age of onset of SAD and more extensive Ramsawh et al., 2011).
psychopathology and global functional impair- The cognitive model of panic (Clark, 1986)
ment in children and adolescents with comorbid proposes that cognitive symptoms related to PD
PD and SAD, suggesting that children with both differ by age and developmental stage. Fear of
SAD and PD likely experience more impairment dying has been reported in children and young
with anxiety, self-criticism, and social interac- adolescents, whereas fear of going crazy and
tions (Doerfler et al., 2008). Given that an esti- depersonalization is more prevalent in older ado-
mated 75% of adults seeking treatment for lescents (Masi et al., 2000a or b). Awareness of
anxiety disorders reported a history of childhood early-onset PD and a more precise definition of
SAD (Manicavasagar et al., 2010), early identifi- early signs and possible clinical subtypes may
cation, diagnosis, and treatment of SAD is reduce clinical impairment and improve the prog-
crucial. nosis of individuals with PD (Masi et al., 2006).
Accurate and timely identification is essential, avoidance of situations or places related to the
given that untreated PD leads to lower quality of panic attack or where escape or obtaining help
life and considerable disability (Comer et al., during an attack is either difficult or embarrass-
2011). Among adults, marital strife, occupational ing (Masi et al., 2006). While PD with AG is
deficiency, poor sense of health, and persistent associated with increased reports of disability
use of medical services are common quality of and impairment among adults (Bonham &
life issues associated with PD, even after symp- Uhlenhuth, 2014), there is little research avail-
tom remission (Davidoff et al., 2011). able regarding comorbidity of AG, related avoid-
Although PD prevalence is low in the child ance behaviors, and symptom severity in children
and adolescent general population relative to and adolescents diagnosed with PD (Kearney
other disorders, a significant proportion of chil- et al., 1997) and even less on children/adoles-
dren and adolescents diagnosed with PD present cents with AG only due to the recent decoupling
with comorbid generalized anxiety disorder from the DSM-IV PD diagnostic category. While
(GAD; Masi et al., 2004), obsessive-compulsive separating AG from PD creates a diagnostic
disorder (OCD; Goodwin et al., 2001; Masi et al., option for characterizing school refusal among
2005), and SAD (Biederman et al., 1997; Bradley youth who do not meet criteria for other disorders
& Hood, 1993; Doerfler et al., 2007; Masi et al., (Chou et al., 2015), there is also evidence to sug-
2000a or b). Though a sole PD diagnosis is not as gest that the revised AG diagnostic criteria may
impairing as social anxiety disorder (see below) leave a considerable proportion of youth experi-
with respect to social functioning in children and encing substantial impairment due to agorapho-
adolescents (Quilty et al., 2003), clinician-ratings bic symptoms without a specified DSM-5 anxiety
reveal that children and adolescents with both PD diagnosis (Cornacchio et al., 2015), potentially
and social anxiety are more severely affected in presenting barriers to service access.
global impairment than children with other anxi-
ety disorders (Last et al., 1992). If untreated, PD
shows the lowest rate of recovery and highest risk Social Anxiety Disorder
of development of new disorders relative to other
anxiety disorders (Last et al., 1996). However, Social anxiety disorder (SA) in childhood is
adolescents suffering from PD may also avoid associated with significant impairment, most
public spaces and engage in school refusal behav- notably in the educational domain, manifesting
ior due to fear of future panic attacks; current primarily through early departures from school,
interventions do not seem to have a significant school refusal, acquisition of lower levels of edu-
positive impact on school attendance in these cational training, and academic underachieve-
cases (Hella & Bernstein, 2012). ment (Keller, 2003; Kessler, 2003; Aderka et al.,
2012). Children with SA exhibit impairment in
their relationships, have fewer peer relationships,
Agoraphobia limited involvement in outside activities, and
more somatic symptoms (e.g., headaches and
Added as a stand-alone diagnosis in the DSM-5 stomachaches) than their counterparts who do
(APA, 2013), agoraphobia (AG) is characterized not carry the diagnosis (Beidel et al., 2000;
by anxiety or intense fear that is triggered by Khalid-Khan et al., 2007). SA affects most areas
exposure (real or anticipated) to at least two of of life, particularly educational attainment,
five specified situational domains: standing in career/work productivity, and development of
line or being in a crowd, being outside of the functional romantic relationships (Wittchen
home, being in open spaces, being in enclosed et al., 2000), also known as romantic competence
places, or public transportation. AG causes clini- (Bouchey, 2007). The level of impairment found
cally significant distress or impairment. When in children and adolescents with SA is particu-
linked to PD, AG may manifest through phobic larly high; evidence suggests it is one of the most
impairing psychiatric disorders (Alonso et al., 2019). Similarly, a study of 594 adolescents ages
2004), affecting primarily social and educational 12–18 revealed a negative relationship between
settings as opposed to the family domain (Aderka social anxiety and social adaptation (Peleg,
et al., 2012). Severe cases of SA may result in 2012). Notably, a positive association between
failure to speak in feared social situations, even if social anxiety and social rejection, and a negative
normative expressive language development is association between social anxiety and social
present, and result in the development of selec- acceptance and popularity was found in 12–13-
tive mutism (Khalid-Khan et al., 2007, see year olds. The same pattern emerged for 14–15-
below). In adolescence and early adulthood, SA year olds, but with a weaker correlation; however,
has been associated with increased rates of acute there was no significant correlation between
suicidal ideation, attempted suicide, and drug and social anxiety and social adaptation for partici-
alcohol dependencies (Keller, 2003; Kessler, pants ages 17–18 years (Peleg, 2012). Higher
2003; Herres et al., 2019; Rapp et al., 2017; levels of social anxiety may lead to avoidance of
Wittchen & Fehm, 2003); SA may be a unique social scenarios and reductions in social connec-
risk factor for active suicidal ideation/attempts tions; peers may not make efforts to initiate
among Latinx adolescents (Rapp et al., 2017). friendships when they observe the anxious ado-
SA is highly comorbid with other anxiety disor- lescents’ avoidance, which in turn increases the
ders, including PD or AG (Sareen & Stein, 2000), adolescent’s sense of social rejection, low popu-
major depressive disorder (MDD) and attention larity, and isolation, leading to further impair-
deficit hyperactivity disorder (ADHD) in addi- ment (Peleg, 2012).
tion to GAD and specific phobias (Chavira et al., Of the anxiety disorders, SA may exert the
2004a or b). greatest impact upon academic functioning (de
SA is the most commonly occurring anxiety Lijster et al., 2018). For example, in the
disorder, with lifetime prevalence rates estimated Netherlands, a nonclinical sample of 312 chil-
between 12% and 13% (Kessler et al., 2005a or b; dren ages 10–12 was assessed via both teacher
Kessler, 2003). SA typically occurs during late and child reports for classroom functioning and
childhood or early adolescence. Epidemiological symptoms severity (Muris & Meesters, 2002).
studies indicate that over 50% of individuals have Using the Spence Children’s Anxiety Scale
retrospectively reported onset by age 13 years (Spence, 1998) with children and a sociometric
(Chavira & Stein, 2002), 75% prior to 16 years, ranking procedure that included teacher assess-
and 90% by age 23 (Kessler et al., 2005a or b). ments of learning attitude, quality of the teacher–
Findings from a 5-year, prospective longitudinal student relationship, quality of peer relationships,
study of 3021 community cases exploring the and self-esteem reports, findings revealed that
evolution of SA revealed that the majority of higher levels of social anxiety symptoms per
cases emerged in the early teenage years, and that child-report were associated with increased dif-
by 19 years of age either a progressive deteriora- ficulties in classroom functioning (including gen-
tion in functioning or a persistent course of ill- eral classroom functioning, greater difficulty
ness had been established (Narrow et al., 2002). with peer relations, and lower self-esteem).
There is evidence to suggest that SA presenta- Similarly, school-aged children with SA feared
tion and associated impairment varies by devel- and avoided a significantly greater number of
opmental stage. Findings of a recent meta-analysis social situations and were significantly more
also indicated that younger adolescents (ages likely to have trouble initiating friendships and to
12–13 years) have higher levels of social anxiety prefer to spend time alone (rather than with peers)
than youth at other ages, and that social anxiety compared to a sample of children carrying a diag-
generally affected social performance/social nosis of GAD (Bernstein et al., 2008). In this
adaptation, defined in this study as self-perceived sample, symptom severity in the sample with SA
social acceptance, self-perceived social rejection, only was inversely associated with greater defi-
and classmate ratings of popularity (Maes et al., cits in social skills, leadership skills, academic
functioning, and directly related to attention dif- 2012), the lack of speech interferes substantially
ficulties and learning problems. Bernstein et al. with social communication and educational func-
(2008) hypothesize that the attention problems tioning, thus presenting substantial impairment
may occur due to distraction by worries about across these domains. Although age of onset is
answering questions in school, fears of reading in typically between 2 and 4 years, on occasion the
front of the class, or fears of talking to peers, and condition may not be detected until elementary
that learning problems may be exacerbated by school (see Viana et al., 2009 for a review). A
anxiety about asking for help, taking tests, or recent meta-analysis revealed exceptionally high
writing/speaking in front of class. rates of SM comorbidity (80%) with other anxi-
DSM-5 modifications to SA, which include ety disorders, most notably SA (69%), followed
removal of the “generalized” SA specifier along by specific phobia (19%), SAD (18%), GAD
with the addition of the “performance-only” SA (6%), and OCD (6%) (Driessen et al., 2020).
specifier, may have unique implications for youth Children with a previous diagnosis of SM often
with impairment due to SA. Among a sample of continue to have communication issues later on
200 youth seeking treatment for SA, Kerns et al. in life (even in adulthood), demonstrating ongo-
(2013) found higher levels of symptom severity ing issues with school or work performance as
and comorbidity in the sample of youth who met well as higher rates of psychiatric disorders
DSM-IV criteria for generalized SA compared to (Muris & Ollendick, 2015).
those with non-generalized SA. Almost twice as
many children met criteria for generalized SA
compared to non-generalized SA, and no youth Specific Phobia
in any group presented with DSM-5 performance-
only SA. Findings are consistent with epidemio- Specific phobia has been found to lead to signifi-
logic studies, indicating that over 50% of youth cant social and academic difficulties due to over-
with SA exhibit fears that are generalized, whelming distress and increase a child’s risk of
whereas less than 1% exhibit performance-only adult psychopathology (Cowart & Ollendick,
fears (Burstein et al., 2011). 2012). Specific phobias often emerge during
childhood but tend to peak during adulthood and
persist into old age, with phobias lingering any-
Selective Mutism where from several years to decades for 10–30%
of individuals (Eaton et al., 2018). Mean age of
Reclassified as an anxiety disorder in DSM-5, onset for specific phobia is 6 years, and children
selective mutism (SM) is characterized by a con- afflicted usually suffer a chronic course of the
sistent failure to speak in specific social situa- disorder if untreated (Wehry et al., 2015).
tions where there is an expectation for speaking Globally, lifetime prevalence rates of specific
(e.g., at school), despite the production of speech phobias range from 3% to 15%, with the most
in other circumstances or situations (APA, 2013). common fears/phobias related to animals and
Children with SM present with a low frequency heights (Eaton et al., 2018; Wardenaar et al.,
of words, low volume, and less spontaneity, 2017). Early age of onset, higher rates of other
which is similar to patterns found in individuals disorders, and more severe symptom severity and
with SA (Muris & Ollendick, 2015), yet distinc- impairment have been found in adolescents with
tions between the two disorders have been found multiple phobias (Burstein et al., 2012). Though
on measures of verbal and nonverbal inhibition less prevalent than other specific phobias, school
(Milic et al., 2020). While epidemiological stud- phobia may be the most noticeable and result in
ies estimate that less than 1% of the population is the most social impairment in a variety of
afflicted with SM and thus it is considered to be domains; children and adolescents suffering from
relatively rare (Bufferd et al., 2011; Chavira school phobia may feel unable to perform class-
et al., 2004a or b; Keeton & Crosby Budinger, room tasks and experience isolation and
a lienation from peers; such perceptions may con- lishing and maintaining healthy peer and family
tribute to prolonged school absence and inhibit relationships, and managing academic tasks.
completion of developmental tasks (Okuyama GAD symptoms can impose marked distress and
et al., 1999). interfere with social, emotional, and educational
Very few studies have examined the frequency, functioning; the disorder has been linked to an
symptom duration, and associated social impair- impaired quality of life across the lifespan, as
ment of specific phobias in child and adolescent well as higher rates of comorbid adult mental
populations. According to findings from a global health disorders (Imran et al., 2017). Though
study of adults, social phobia was accompanied most people with GAD experience symptoms
by severe role impairment reported in 18.7% of onset in late adolescence, their 20s, or early 30s
cases, with the lowest level of severe impairment (Wittchen, 1994; Beesdo et al., 2010), childhood
in the relationship domain (7.9%) and the highest GAD afflicts approximately 10–15% of the pop-
level in the home domain (10.3%) (Wardenaar ulation with a mean age of onset of 8.8 years
et al., 2017). While functional impairment may (Last et al., 1992; Costello et al., 2005a or b).
be at least partially due to a restricted lifestyle While GAD affects approximately 1% of chil-
caused by the hallmark fear and avoidance related dren and 3% of adolescents in the general popu-
to specific phobias (Wardenaar et al., 2017), other lation (Burstein et al., 2014; Gale & Millichamp,
studies have suggested that a high rate of co- 2016), prevalence rates are as high as 59% in
occurrence with other disorders may account for child anxiety clinics, and between 1 and 10% in
some of the observed functional impairment in general child psychiatric clinics (Imran et al.,
specific phobia (Comer et al., 2011). 2017).
Essau et al. (2000) report that in a clinical Common themes of worry in children with
population of adolescents meeting criteria for GAD include perfectionism, punctuality, health
specific phobia, the most frequent phobia and safety of themselves and others, catastrophic
reported was blood (39.6%), followed by animals world events (e.g., weather disasters, war), fam-
(28%), natural environments (26%), and specific ily finances, and events in the distant future (e.g.,
situations (23.7%). Panic symptoms were signifi- college) (Layne et al., 2009). Though children
cantly associated with each phobia during the with GAD exhibit age-appropriate worries (e.g.,
worst episode, the most frequent of which were grades, homework, friends), such worries occur
that of palpitation, trembling/shaking, and sweat- in excess of peers their same age. In one nonclini-
ing. All cases with any subtype of specific phobia cal sample of children ages 8–13, children who
were impaired in school, leisure, and social activ- met criteria for GAD or overanxious disorder
ities during the worst episode of their disorder (OAD) endorsed an average of six worries com-
(Essau et al., 2000). Given that it may be possible pared to control children who endorsed an aver-
to interrupt the developmental course of phobias age of only one worry (Muris et al., 1998). In the
when a clear progression from fear to avoidance, same study, children meeting criteria for GAD/
and finally to diagnosis can be observed (Eaton OAD could also be distinguished from control
et al., 2018), future research should focus on children due to a higher frequency of their pri-
early identification and intervention strategies. mary worry, a stronger degree of interference in
daily functioning, and more difficulty controlling
their worry, indicating that frequency and inten-
Generalized Anxiety Disorder sity of worry differentiate children with GAD
from those carrying other anxiety disorder diag-
Children presenting with generalized anxiety dis- noses. Worries can translate into worry behav-
order (GAD) have been characterized as “worri- iors, such as avoidance of potentially negative
ers” and “little adults” due to their excessive, events or activities, procrastination in either
adult-like worries. Their worries can interfere decision-making or behavior, and extensive time
with accomplishing daily responsibilities, estab- spent in preparing for potentially negative
o utcomes of events or activities (Andrews et al., 12–17 years) with GAD reported more somatic
2010). symptoms than younger children (ages
Though three (of the six) associated symp- 5–11 years) and somatic symptom incidence was
toms listed in criterion C of the DSM-5 (i.e., rest- reported more frequently among children with
lessness, fatigue, concentration difficulty, GAD than among those without the diagnosis
irritability, muscle tension, sleep disturbance) are (Ginsburg et al., 2006). Somatic symptoms were
required for a diagnosis of GAD in adults, only significantly associated with anxiety severity,
one is required for diagnosis in children (APA, impaired global functioning, avoidance, and
2013). A number of studies, however, indicate interference with family relationships; however,
that children diagnosed with GAD commonly the presence of somatic symptoms was not asso-
endorse more than one symptom. One study ciated with impaired peer relationships (Ginsburg
revealed that a sample of children with GAD et al., 2006).
endorsed an average of 3.4 associated symptoms, The differential worry content evident in chil-
with restlessness the most common (74%) and dren with GAD has implications for social func-
muscle tension the least common (29%) (Tracey tioning. Though results of one study exploring
et al., 1997). A subsequent study of 47 children the presentation of GAD in a nonclinical sample
diagnosed with GAD (ages 9–13 years) revealed of children (7–11 years old) indicate that the
a consistent pattern of symptom presentation most common domain of worry endorsed both by
(Kendall & Pimentel, 2003). Both studies children with GAD (as well as anxious children
revealed that the number of associated symptoms without GAD) was the health of significant oth-
increased with age. A more recent study compar- ers (55 and 45%, respectively), children with
ing children with GAD to anxious children with- GAD were significantly more likely to worry
out GAD revealed similar results; children with about their performance and family issues than
GAD reported an average of 3.4 associated were children without GAD diagnosis (Layne
symptoms whereas anxious children without et al., 2009). These results are consistent with the
GAD reported significantly fewer associated characterization that children with GAD are
symptoms (Layne et al., 2009). Consistent with excessively preoccupied with grades, how they
previous research, the most common associated are perceived by others, and family matters.
symptoms reported by children with GAD Results of another study of school-aged children
included restlessness/trouble relaxing, trouble revealed a GAD diagnosis to be positively related
concentrating, and trouble sleeping with 67% of to stronger social skills and negatively related to
children reporting these symptoms. attention problems when compared to a sample
Though worries of children and adolescents of children with SA (Bernstein & Layne, 2006).
with GAD are characterized by continuous self- The authors hypothesize that this association
doubt, elevated sensitivity to criticism, and may be due to the fact that GAD in children is
chronic need for reassurance (Wagner, 2001), often characterized by a perfectionism, an overly
they are more often accompanied by somatic conscientious work ethic and an eagerness to
symptoms or physical complaints. Physical com- please others, especially adults (Bernstein &
plaints were reported in over 70% of subjects in a Layne, 2006).
sample of 58 children diagnosed with GAD Like SA, GAD is also highly comorbid with
(Masi et al., 1999a or b). In a subsequent study of other psychiatric disorders (Masi et al., 2004;
162 clinically referred children, those with anxi- Layne et al., 2009). In the study by Layne et al.
ety and/or depression reported significantly (2009), only 14% of participants carried GAD as
higher rates of somatic complaints, most often their only diagnosis; 63% of the sample carried
headache, than subjects with other mental disor- comorbid anxiety diagnoses. Masi et al. (1999a or
ders (Masi et al., 2000a or b). Additional research b) note that co-occurrence with specific phobia,
indicates that severity of somatic symptoms may SAD, and SA is more often the rule than the
increase with age; older children (ages exception; several studies reveal that up to 60%
of anxious children meet criteria for two of the have been reclassified into new diagnostic cate-
aforementioned three disorders and 30% meet gories of obsessive-compulsive and related disor-
criteria for all three (e.g., Birmaher et al., 2003). ders (OCRD) and trauma- and stressor-related
Similarly, in the clinical sample of Masi et al. disorders, respectively (APA, 2013). While a
(2004), the prevalence of a stand-alone GAD review of all OCRD and trauma- and stressor-
diagnosis was 7%; 75% were diagnosed with at related disorder impairment is beyond the scope
least one other anxiety disorder. Results of a of this chapter, high comorbidity rates of OCD
study examining impairment in children ages (e.g., Storch et al., 2008) and PTSD (e.g.,
6–11 years who were classified into one of three Galatzer-Levy et al., 2012) with DSM-5 anxiety
groups (“pure” GAD, comorbid GAD, and disorders remain prevalent and associated with
“healthy” controls) showed that both clinical greater functional impairment and disability, and
groups were significantly less adaptive in the thus, are reviewed briefly here. In addition, diag-
family domain, but those in the comorbid group noses of depression, autism spectrum disorder
evidenced higher levels of impairment across all (ASD), and ADHD also evidence increased
domains (Alfano, 2012). social and functional impairment when co-
There is some evidence to suggest that the occurring with anxiety disorders and are
type of disorder that co-occurs with GAD varies described briefly below.
with age, with younger children (5–11 years) Frequently characterized by prominent avoid-
more likely to experience co-occurring SAD or ant behaviors and increased family accommoda-
attention deficit hyperactivity disorder, whereas tion (e.g., Lebowitz et al., 2016), pediatric OCD
older children (12–19 years) more frequently in particular is associated with a chronic yet fluc-
experience comorbid MDD or simple phobia tuating course that both confers heightened risk
(Strauss et al., 1988a or b or c). Older children for later psychiatric and psychosocial morbidity
with GAD also reported significantly higher and causes significant impairment at home, at
severity of anxiety and depression symptomol- school, and in social settings (Krebs & Heyman,
ogy and a higher total number of anxiety symp- 2014). As Piacentini et al. (2003) note, difficul-
toms on self-report measures, indicating that ties with tardiness to school or bedtime routines
manifestation of GAD impairment varies by may be due to compulsions around bathing and
developmental stage (Strauss et al., 1988a or dressing. Eating in restaurants and attending pub-
b, or c). Other research indicates that intensity of lic places may be inhibited by contamination
symptoms also differentiates children with GAD concerns. Attention and concentration associated
versus simple phobia (Weems et al., 2000), but with reading, listening, having a discussion,
that the most common comorbid disorders are school-related tasks (e.g., doing homework) may
social phobia and SAD (Keeton et al., 2009). be impaired by counting rituals, negative intru-
sive thoughts, and/or checking and repeating
compulsions. The ability for youth to develop
ritical Considerations and Future
C friendships and romantic relationships may also
Directions be hindered by severe OCD symptoms (Piacentini
et al., 2003).
Comorbidities and Related Disorders Pediatric OCD has a significant effect on the
emotional well-being of family members them-
While anxiety disorders frequently co-occur with selves. Caregivers of youth diagnosed with OCD
one another, there is extensive evidence to indi- report high levels of stress, anxiety, and sadness;
cate high levels of comorbidity with disorders in youth suffering from OCD report high levels of
other DSM-5 diagnostic classification categories. frustration and anger, suggesting that OCD
Two disorders previously categorized as DSM-IV causes significant impairment in overall quality
anxiety disorders, obsessive-compulsive disorder of life and family functioning (Coluccia et al.,
(OCD) and posttraumatic stress disorder (PTSD), 2017; Stewart et al., 2017). Unsurprisingly,
f amily impairment has been associated with fam- these circumstances may manifest differentially.
ily accommodation, with specific obsessions For example, the presence of at least one anxiety
(contamination and religious) associated with disorder occurs in approximately 40% of youth
greater symptom severity (Stewart et al., 2017). presenting with ASD and is generally associated
These results corroborated previous research that with increases in repetitive behaviors, resistance
indicated family accommodation is not only to change, and social skills deficits (Zaboski &
common but also associated with more severe Storch, 2018). Comorbid anxiety in youth with
symptoms, additional impairment, and less posi- ASD has also been associated with more frequent
tive treatment outcomes (e.g., Peris et al., 2012; occurrence of self-injurious behaviors, depres-
Peris & Piacentini, 2013; Storch et al., 2007, sion, and increased parental stress (Kerns et al.,
2012). 2015). In particular, SA frequently co-occurs
Although less well-studied, family accommo- with ASD, and has been found to negatively
dation is also associated with PTSD (see Reuman impact social motivation, social skills, and func-
& Thompson-Hollands, 2020 for a review). tioning (Spain et al., 2018). While social impair-
While a relatively small proportion of individuals ments associated with ASD could actually
who have experienced trauma develop PTSD (see contribute to the development of SA, as certain
Bonanno et al., 2015 for a review), anxiety sensi- symptoms (e.g., social withdrawal) may result
tivity (AS), defined as the fear of anxiety-related from challenges with social communication, it is
sensations due to beliefs that such sensations will also possible that certain core symptoms of ASD
yield negative social, psychological, and physical (e.g., impairments in social interactions or for
outcomes (Reiss & McNally, 1985), has been example reduced eye contact) could be miscon-
shown to be associated with increased PTSD strued as SA symptoms (Briot et al., 2020).
symptom severity in youth who have experienced Similarly, anxiety disorders, which may affect
a traumatic event (Leen-Feldner et al., 2008; approximately 25–33% of youth with ADHD,
Kılıç et al., 2008). Adverse childhood events have a significant impact on the clinical presenta-
(ACEs) are highly prevalent among adults with tion, prognosis, and treatment outcomes of
anxiety disorders (van der Feltz-Cornelis et al., ADHD (Biederman et al., 1991; Jensen et al.,
2019), with sexual abuse and family violence in 1997; March et al., 2000; D’Agati et al., 2019).
childhood posing the greatest risk for later anxi- While it is possible that impaired concentration
ety disorder development (see De Venter et al., due to anxiety may be misdiagnosed as ADHD
2013 for a review). (Abramovitch et al., 2013), children with comor-
In addition to extant research documenting bid ADHD and anxiety present with increased
comorbidity with depressive and other mood dis- impairment and lower levels of social compe-
orders (e.g., Cummings et al., 2014), there is evi- tence compared to children who only have anxi-
dence to suggest that the extent of comorbid ety or ADHD (Bowen et al., 2008). In a study of
anxiety and depression is underestimated in 310 youth (ages 10–14) with ADHD, symptoms
youth, despite its association with greater symp- of social anxiety and anhedonia were found to be
tom severity, distinctive presentations, and treat- associated with lower levels of social acceptance
ment challenges (Melton et al., 2016). Family and diminished social skills (Becker et al., 2014).
factors may play an important role, as findings Comorbid ADHD and anxiety have also been
from a clinic-based sample of 193 youth present- associated with higher levels of oppositional defi-
ing with comorbid anxiety and depression ant and conduct disorder symptoms in children
reported higher levels of family dysfunction than with comorbid anxiety and ADHD compared to
youth with only anxiety (Guberman & Manassis, counterparts with ADHD or anxiety alone, per
2011). parent and teacher reports (Humphreys et al.,
Studies also indicate a high prevalence of 2012).
comorbidity with anxiety among youth with ASD In addition to disorders reviewed above,
and ADHD in particular, and that impairment in examination of social impairment among other
disorders in both the OCRD and trauma- and Anxiety and Developmental Stages
stressor-related disorders classification catego-
ries is warranted. Given the prevalence of comor- In order to develop effective intervention and pre-
bidities with disorders in other DSM-5 diagnostic vention tools, an understanding of specific risk
classification categories and the associated bur- and protective factors across developmental
den of impairment, future research on anxiety stages is necessary. Depending on the child/ado-
interventions should include samples of children lescents’ age and stage of development, specific
and youth with comorbid diagnoses and address symptoms may cause impairment in particular
social impairment specifically (Sciberras et al., domains and the degree of impairment may
2014). increase or diminish. Specifically, a study exam-
ining the developmental trajectories of specific
anxiety disorders (i.e., SAD, social phobia, GAD,
Subthreshold Anxiety PD, OCD) among a community-based sample of
children and adolescents over a 5-year period
Anxiety-related impairment extends beyond found that anxiety seems to diminish in early
disorder-specific anxiety. While the discussion of adolescence and then slightly increase during
impairment in this chapter has focused on impair- middle (i.e., separation anxiety, social anxiety,
ment within the context of specific anxiety disor- GAD) and late adolescence (i.e., PD, OCD),
ders, subthreshold levels of anxiety have also beyond the effects of depression (Van Oort et al.,
been associated with impairment and distress. 2009). Other studies have shown that, while the
Common in both childhood and adolescence, prevalence of SAD and select specific phobias
subthreshold anxiety symptoms cause marked tend to decrease with age, SA, GAD, PD, and AG
and daily impairment and distress (Ollendick & are significantly more prevalent in adolescents
Hirshfeld-Becker, 2002; Van Oort et al., 2009). (ages 13–18) compared to younger children (see
There is evidence to suggest that symptom onset Beesdo et al., 2009).
may be predicted as early as the preschool years As noted in the disorder-specific and comor-
by inhibited temperament and maternal over- bidities sections above, there are particular devel-
involvement (Hudson et al., 2018), with early opmental considerations relevant to each of the
behavioral inhibition identified as a risk factor for anxiety disorders with regard to assessment,
SA and SAD specifically (Hirshfeld-Becker symptom manifestation, and functional out-
et al., 2007; Garcia-Lopez et al., 2020). Other comes, all of which have implications for treat-
research indicates that subclinical or subthresh- ment and the extent to which family members are
old levels of SA, OCD, and PD predicted full involved. Given the substantial evidence that
onset of the disorders within 7–9 years (Wolitzky- childhood anxiety disorders predict the presence
Taylor et al., 2014). These results are consistent of anxiety and other mental health problems in
with previous research, indicating that individu- adolescence and adulthood and the considerable
als with subthreshold conditions in childhood impairment that accompanies these disorders, it
suffer from impairment and increased risk for is crucial to understand more about the develop-
continuing mental health problems, including mental trajectory of anxiety to inform interven-
disorder development (Angold & Costello, 1996; tion and prevention efforts (Allan et al., 2013;
Gonzales et al., 1994; Sherbourne et al., 1994.; Bittner et al., 2007; Gregory et al., 2007; Brückl
Spitzer, 1995; Valleni-Basile et al., 1996; et al., 2007; Lewinsohn et al., 2008; Haller et al.,
Williams et al., 1995). Given the persistent and 2015; de Lijster et al., 2019).
debilitating course of anxiety disorders, it is criti-
cal to enhance prevention and early detection
efforts to minimize progression of associated
impairment.
Anxiety Measures and Impairment (COIS-R; Piacentini et al., 2003, 2007) assesses
specific functional impairment among children
While substantial evidence demonstrates that and adolescents with OCD.
anxiety impairs children’s global functioning, it Several clinician-administered tools such as
is imperative that there are developmentally sen- the Pediatric Anxiety Rating Scale (PARS;
sitive instruments to assess specific areas of Research Units on Pediatric Psychopharmacology
impairment. A number of assessment tools for Anxiety Study, 2002) assess anxiety over the past
childhood anxiety disorders have been developed week and associated symptoms and impairment.
(e.g., Merlo et al., 2005; Silverman & Ollendick, In addition, the GAD section of the ADIS-5
2005) such as the Multidimensional Anxiety (Brown & Barlow, 2014) includes clinician,
Scale for Children – 2nd Edition (MASC 2; child, and parent impairment ratings based on the
March, 2013), the Modified State-Trait Anxiety child’s report of how their GAD worry negatively
Inventory for Children (STAIC-M; Spielberger, impacted time with friends, in school, and at
1973), Revised Children’s Manifest Anxiety home, as well as the extent to which one engages
Scale – second Edition (RCMAS-2; Reynolds & in specific worry behaviors initially proposed for
Richmond, 2008), the Screen for Child Anxiety inclusion in DSM-5 (see Andrews et al., 2010),
Disorders (SCARED; Birmaher et al., 1999), and but ultimately not adopted.
the Fear Survey Schedule for Children – Revised To date, only three large scale reviews of
(FSSC-R; Ollendick, 1983). These anxiety mea- social functioning measures for children and ado-
sures tend to focus on symptom severity, differ- lescents have been conducted. Orvaschel and
ential diagnosis, and evaluation of treatment Walsh (1984) reviewed a total of 31 “adaptive
outcomes, with limited attention to impairment functioning” instruments for use with preschool
or specific anxiety disorders in detail (Piacentini and school-aged children. Canino et al. (1999)
et al., 2007). More recently, the Youth Anxiety examined 13 measures of “functional impair-
Measure for DSM-5 (YAM-5; Muris et al., 2017), ment” categorized by global impairment,
which includes both parent and child self-reports, domain-specific measures, and symptom-specific
has been developed to assess anxiety symptoms measures. The systematic review conducted by
according to DSM-5 diagnostic classifications. Crowe et al. (2011) revealed 86 measures of
Measurement of anxiety-related impairment “social functioning” in children and adolescents.
in children and youth is relatively limited. While none of these reviews focused on anxiety-
Whiteside (2009) developed a three-item adapta- related impairment exclusively, findings from all
tion of the Sheehan Disability Scale (Sheehan reviews underscored the need for development of
et al., 1996), in which children and parents use a more appropriate measures of impairment that
0–10 scale to rate the degree to which the child’s (1) differentiate symptom severity from func-
symptoms interfere with general functioning at tional impairment in children, (2) clarify the rela-
home, at school/work, and with friends. tionship of anxiety to normative developmental
Originally developed to assess anxiety-related functioning, and (3) consider a child’s ability to
functional impairment in school, social, and fam- adapt to varying demands occurring within
ily domains, the Child Anxiety Impact Scale – domains of home, school, community, and inter-
Parent Version (CAIS-P; Langley et al., 2004) personal peer relationships. It is also very impor-
has been modified in recent years; in addition, the tant that measures of impairment include a
authors developed a child version (CAIS-C; breadth of domains and problems across child
Langley et al., 2014) to address the frequently and adolescent development, and a number of
occurring problem of inconsistent reports versions capturing multiple perspectives (e.g.,
between child-ratings of their anxiety-related child, caregiver, teacher) in order to more accu-
impairment and parent-ratings of their child’s rately evaluate specific manifestations of impair-
anxiety (e.g., Choudhury et al., 2003; Piacentini ment and the extent to which it occurs.
et al., 2003). The Child OCD Impact Scale
COVID-19 and Sociocontextual pate, understand, and address potential

Factors impairment as early as possible.
Although there is substantial evidence docu-
Risk and protective factors for anxiety-related menting associations between both direct expo-
impairment may also manifest differentially sure to discrimination and worsening mental
across population subgroups and in response to health symptoms (e.g., Cuevas et al., 2020;
sociopolitical phenomena. Although there is Cuevas & Boen, 2021; Priest et al., 2013; Priest
some evidence to suggest that the COVID-19 & Williams, 2018; Williams et al., 2018) as well
pandemic has exacerbated rates of anxiety and as adverse effects of secondary exposure to racist
depression in children and adolescents (Courtney discrimination among children and youth specifi-
et al., 2020), the long-term impact that the pan- cally (e.g., Heard-Garris et al., 2018), most stud-
demic has had on anxiety-related social impair- ies on anxiety disorders and related impairment
ment in youth, both across various developmental in children and adolescents have failed to
stages and with respect to specific anxiety and acknowledge the complexity of racism and cul-
related disorder trajectories, is not yet evident. tural exclusion that may influence development
Given that handwashing and other forms of per- of anxiety disorders, anxiety-related impairment,
sonal hygiene have been so heavily emphasized and disability over time. While a few studies do
as an important protective tool against the spread report cultural phenomena in relation to child
of COVID-19 infection, it will be important to anxiety symptoms (e.g., parental acculturative
examine the extent to which these behaviors stress – see Leon, 2014) or examine anxiety in
manifest in relation to germ phobia or relation to post-migration adjustment among
contamination- related obsessions and compul- undocumented adults (e.g., Garcini et al., 2017),
sions. Similarly, it will be essential to differenti- most studies of youth do not examine or report
ate behaviors consistent with appropriate public variation in anxiety-related social impairment
health social distancing precautions from those among racial subgroups, assess or measure dis-
that might be clinically significant and/or warrant crimination within the context of other mecha-
an AG diagnosis. In a similar vein, the social iso- nisms of racism, or account for ways in which
lation accompanying necessary public health pre- sociopolitical phenomena may be experienced
cautions such as quarantines, lockdowns, school differentially and contribute to anxiety-related
closures, and other mitigation measures designed impairments in social functioning. Given that
to slow the spread of COVID-19 may have there is some evidence for differential anxiety
impacted social adaptation by limiting opportuni- symptom trajectories among youth by race (e.g.,
ties for socialization at critical developmental Arora et al., 2017), ethnicity (e.g., Okamura
points for many children and adolescents (Singh et al., 2016), and by race in response to negative
et al., 2020). Early studies on the impact of the life events specifically (see Lewis et al., 2012), it
pandemic on child and adolescent mental health is imperative that investigations of anxiety-
have revealed reduced affect in children due to related impairment and social disability both
feeling deprived of opportunities to meet friends, measure and account for these factors.
play outdoors and participate in school activities
in person, higher levels of attention-seeking,
“clingy” behaviors, and dependence on parents Summary
(Lee, 2020; Liu et al., 2020; Zhai & Du, 2020).
While findings suggest that the pandemic may This chapter provides a review of the literature
yield higher rates of anxiety and related disor- focused on impairment related to childhood anxi-
ders, particularly among youth belonging to com- ety disorders. While anxiety disorders are highly
munities disproportionately impacted by the prevalent and known to be disabling, there is still
pandemic and/or who have lost a parent or care- limited research in the area of impairment, which
giver to COVID-19, it will be important to antici- is due, in part, to the availability of relevant
easures. It is essential that development be an

m Allan, N. P., Capron, D. W., Lejuez, C. W., Reynolds,
E. K., MacPherson, L., & Schmidt, N. B. (2013).
important consideration when assessing impair- Developmental trajectories of anxiety symptoms in
ment, as a child’s level of functioning is appropri- early adolescence: The influence of anxiety sensitiv-
ate at specific periods of development, but not ity. Journal of Abnormal Child Psychology, 42(4),
others (Hoagwood et al., 1996). Assessing anx- 589–600. https://doi.org/10.1007/s10802-013-9806-0
Alonso, J., Angermeyer, M. C., & Lepine, J. P. (2004).
ious children and adolescents’ functional level The European Study of the Epidemiology of Mental
and ability to negotiate their environments are Disorders (ESEMeD) project: An epidemiological
key to determine the need for treatment basis for informing mental health policies in Europe.
(Hoagwood et al., 1996), prevent possible dete- Acta Psychiatrica Scandinavica, 109(s420), 5–7.
https://doi.org/10.1111/j.1600-0047.2004.00325.x
rioration, and inhibit the development of addi- American Psychiatric Association. (2013). Diagnostic
tional mental health problems. Future research and statistical manual of mental disorders (5th ed.).
must include measures of social impairment https://doi.org/10.1176/appi.books.9780890425596
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K., Craske, M. G., Heimberg, R. G., Rapee, R. M.,
caused by different anxiety disorders in more Ruscio, A. M., & Stanley, M. A. (2010). Generalized
detail and with greater specificity, and account worry disorder: A review of DSM-IV generalized
for sociopolitical contexts in which these impair- anxiety disorder and options for DSM-V. Depression
ments occur. Future research on anxiety-related and Anxiety, 27(2), 134–147. https://doi.org/10.1002/
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impairment for children versus adolescents, and ing an empirical basis for the diagnosis of oppositional
whether differences exist based on environmental defiant disorder. Journal of the American Academy of
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https://doi.org/10.1097/00004583-199609000-00018
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examine impairment in relation to environmen- dictor of depressive symptoms among Asian American
tal/contextual factors (including both sociocul- early adolescent youth: The role of parent, peer, and
teacher support and school engagement. Cultural
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Index
A C
Accommodation, 37, 126, 130, 219, 237, 251, 260, 289, Categorical, 29, 38, 39, 85, 97, 99–103, 105–107, 111,
293, 300, 307, 333–338, 341, 388, 395–406, 412, 113, 115, 120, 142, 145, 203, 204, 207, 212,
419, 434 290–292
Adolescence, 10, 13–15, 30, 37, 75, 97, 105, 129, 142, Categories, 4, 7, 11, 15, 22, 29–31, 39, 47–49, 60, 61,
143, 146, 158, 160, 161, 163, 164, 166, 184, 194, 97, 100, 101, 103, 105, 111–113, 115–117, 120,
197, 203, 209–211, 221, 274, 282, 287, 299, 300, 125, 128, 133, 177, 185, 204, 207, 209, 212, 238,
332, 367, 369, 370, 380, 446, 447, 449, 451, 455 273, 287, 331, 352, 397, 446, 448, 453, 455
Anxiety, 3–9, 11–22, 29–39, 45–52, 55–66, 73–86, Categorization, 39, 103
97–107, 111–120, 125–133, 141–151, 157–166, Children, 3–22, 29–33, 35–38, 46–52, 60, 73–75, 78, 79,
173–186, 191–199, 203–212, 217–227, 237–239, 81, 83, 84, 97–107, 111–120, 125–133, 141–151,
241, 242, 249–262, 271–282, 287–289, 294–296, 157–166, 174, 176–186, 191–199, 204–211,
299–309, 316, 321, 323, 333, 337–339, 347–353, 217–227, 235–245, 249–262, 271–282, 287–296,
357–362, 379–389, 395–406, 411–420, 425–438, 299–309, 315–324, 331–341, 347–353, 360,
445–458 367–375, 379–389, 395–405, 411–419, 425–438,
Anxious arousal, 116, 181, 238 445–458
Assessment, 3, 4, 6–8, 18, 29, 37, 39, 48, 49, 82, 97, Children’s Yale-Brown-Obsessive-Compulsive Scale
111–113, 115, 117, 118, 129, 130, 141, 148, 150, (CY-BOCS), 38, 335, 383, 384
164, 165, 174, 178, 195, 197, 199, 208, 209, 211, Classification, 3–6, 38, 39, 97–99, 111, 112, 120, 193,
218, 226, 237–245, 251–253, 257, 259, 262, 203, 204, 301, 315, 453, 455, 456
271–273, 275, 280, 282, 294, 295, 299–302, 306, Cognition, 30, 32, 33, 35, 38, 47, 48, 50, 51, 65, 98, 126,
308, 335–338, 341, 350, 373, 380, 381, 383, 384, 129, 148, 181, 183, 193, 226, 236, 238, 240–243,
387, 389, 399, 400, 419, 435, 449, 455, 456 260, 273, 274, 280–282, 299, 303, 315, 316, 323,
Attention deficit hyperactivity disorder (ADHD), 8, 37, 336, 382, 412, 430
65, 79, 83, 126, 127, 141–151, 262, 272, 333, Cognitive-behavioral therapy (CBT), 6, 37, 82, 130–132,
334, 351, 379, 449, 453, 454 148, 149, 198, 199, 224–226, 239–243, 245,
Autism spectrum disorder (ASD), 79, 80, 83, 98, 143, 259–262, 271, 273–282, 288, 294, 296, 305,
237, 272, 379–389, 453, 454 307–309, 315–318, 320–322, 324, 337, 338, 340,
Aversions, 174, 177, 178, 185, 368, 370–372, 374, 375 341, 347, 348, 353, 370, 375, 385–387, 401–405,
Avoidance, 5, 8, 12–15, 18–21, 30–32, 36, 37, 39, 47, 411, 413, 415–419, 426, 428–434, 437
50, 59, 62, 98, 100, 106, 126–131, 146, 158, 159, Cognitive errors, 45–47, 49, 51
162, 164, 173, 174, 176–178, 180, 181, 183–186, Common elements, 133
192, 193, 209, 219, 220, 222, 224, 225, 236, 237, Communication, 21, 125, 223, 226, 289, 293, 296, 317,
239, 240, 250, 252, 253, 257, 262, 282, 288, 289, 334, 335, 379, 380, 382, 384–388, 395, 396, 401,
293, 299–304, 309, 315, 316, 318, 333–337, 402, 404, 413, 415, 417, 419, 450, 454
367–370, 372–375, 380, 384, 385, 388, 398, Communities, 4, 8, 9, 11, 14, 17, 49, 79, 101, 103–105,
412–414, 431, 434, 446, 448, 449, 451, 452 113, 130, 157, 163, 185, 186, 203, 208–210,
223, 237, 244, 245, 252, 256, 261, 273, 282,
289, 290, 292, 306, 308, 320–324, 350, 369,
B 384, 411, 418, 419, 425, 430, 431, 436–438,
Biology, 3 449, 456, 457
© The Editor(s) (if applicable) and The Author(s), under exclusive license to 469
Springer Nature Switzerland AG 2023
https://doi.org/10.1007/978-3-031-14080-8
470 Index
Comorbidity, 8, 9, 14, 19, 22, 29, 30, 32, 38, 47–49, F

65, 77, 98, 106, 111, 113, 114, 116, 125–129, Families, 8, 11, 30, 31, 64, 73–78, 80, 83, 98, 116, 130,
133, 143, 157–162, 164–166, 203, 204, 146, 147, 150, 160, 164, 178, 217, 219, 225, 226,
206–210, 212, 237, 242, 259, 272, 287, 295, 235, 236, 239, 243, 245, 249–252, 260, 261, 271,
332, 333, 352, 360, 381, 445, 446, 448, 450, 273, 279, 280, 287–289, 292, 293, 304, 306, 317,
453–455 319–324, 333–339, 341, 352, 353, 360, 385–389,
Conceptualization, 5, 19, 29, 30, 47, 50, 82, 97, 100, 395–406, 411–420, 425, 426, 429, 434, 436, 437,
112–118, 120, 129–132, 173, 178, 182, 184, 191, 445, 446, 449, 451–456, 458
195, 197, 203–208, 212, 218, 272, 280, 287, 288, Family accommodation, 130, 251, 260, 333–337,
293, 301, 337, 368, 413 341, 388, 395–397, 399–402, 404–406, 417,
Content-specificity, 47–49, 51, 52 453, 454
Coronavirus disease-19 (COVID-19), 457 Food, 174, 176–180, 185, 289, 291, 334, 340, 367–375,
405, 431
Food neophobia, 367–375
D
Depression, 32–34, 37, 38, 47, 49, 51, 56, 57, 60, 74,
78–81, 100, 102, 106, 111, 113–118, 126, 127, G
130–132, 157–166, 204–206, 209, 211, 237, 242, Gene modeling, 86
250, 252, 254, 260, 272, 277–279, 282, 299–301, Generalized anxiety disorder (GAD), 8, 17, 29–39,
319, 321, 323, 333, 349, 360, 362, 382, 383, 400, 48–50, 55, 56, 58, 75, 78, 84, 98, 101, 113,
427, 437, 447, 449, 452–455, 457 115, 116, 126, 128, 130, 131, 142–145,
Desensitization, 59, 182, 239, 240, 274, 303–304, 157–160, 163, 206, 208, 223, 235, 237, 251,
317, 318 253, 254, 256, 259–262, 271–282, 300, 304,
Diagnosis, 3–5, 7–22, 29–39, 49, 56, 58, 60, 63, 78, 347–351, 357, 362, 379, 416, 433, 448–453,
80, 83, 97, 98, 100, 102, 111–120, 125, 126, 455, 456
129, 131, 141, 145, 158, 159, 164, 165, 184, Genetics, 5, 11, 12, 38, 62, 63, 66, 73–79, 81–86, 98,
198, 203, 204, 207–209, 212, 221, 226, 113, 127, 160, 161, 178, 192, 217, 238, 250, 300,
237–239, 249, 251, 252, 254, 259, 271, 272, 331–333, 369, 412
275–279, 288, 291, 295, 302, 306, 309, 332, Genomes, 77, 80, 81, 85, 86
333, 347, 349, 350, 357, 360–362, 379, 381, Glutamate, 57, 59, 64, 65, 76, 77, 84, 359, 362
384, 386, 405, 415–417, 429, 432, 433, 437,
447–453, 455–457
Dimensional, 21, 38, 39, 47, 74, 75, 78, 85, 99–106, H
111–120, 145, 203–208, 211, 212 Higher-order factors, 116, 127, 158, 181
Disgust, 12, 102, 105, 173–186, 372–374
Disorders, 3–22, 29–39, 45–52, 55–66, 73–86, 97–107,
111–120, 125–133, 141–151, 157–166, 173–186, I
191–199, 203–212, 217–226, 235, 237–239, 242, Impairments, 8–10, 16, 30, 32, 35, 39, 73, 98, 99, 106,
249–262, 271–280, 282, 287–289, 294–296, 116, 117, 126, 130, 141, 143, 148, 160, 164, 165,
299–303, 305, 307–309, 315, 316, 331–341, 203, 204, 249–252, 259, 262, 272, 274, 288, 295,
347–353, 357–362, 370, 379–381, 383–385, 388, 299, 308, 315, 331–336, 341, 370, 371, 379, 380,
395, 397, 399, 401–406, 411–418, 425, 427–429, 383, 384, 388, 398, 401, 415, 417, 425, 430,
431–438, 445–458 445–458
Diversity, 66, 85, 368, 370, 438 Intellectual disability (ID), 150, 379, 380, 382–384,
Dysfunction, 46, 47, 55, 59, 64, 65, 148, 149, 158, 163, 386–389
164, 204–206, 211, 320, 321, 335, 360, 361, Intellectual functioning, 379, 380, 383, 388
395–406, 418, 454 Interventions, 4, 36, 45, 47, 51, 61, 65, 66, 97, 106,
111, 120, 125–127, 129–133, 148, 149, 151,
164–166, 186, 191, 199, 207, 220, 224–227,
E 240, 241, 245, 250, 260–262, 274, 280, 282,
Ecological momentary assessment (EMA), 195, 197 288, 289, 293–296, 299, 300, 305–309, 315,
Emotional avoidance, 369–377 317–322, 340, 341, 347, 359, 360, 362, 370,
Emotion regulation, 127–129, 131, 191–199, 219, 221, 371, 379, 380, 385–389, 399, 405, 411–415,
250, 304, 379, 401 417–420, 425–438, 448, 451, 455, 458
Exposure and response prevention (ERP), 338–341, 385, Intrusive images, 30, 34, 35, 39
386, 419
Exposure therapy (ET), 61, 303, 304, 316, 321,
338, 385 L
Extinction learning, 61, 339, 358, 359, 362 Linguistics, 295
Index 471
M 396–405, 411–420, 427–431, 433–436, 446, 454,

Mapping, 51, 78 456, 457
Mechanisms, 3, 36, 51, 57, 60, 61, 63, 85, 98, 100, 125, Personality, 114, 116, 118, 120, 127, 131, 141, 203–212,
127–131, 133, 141, 146, 148, 149, 159, 162, 165, 219, 220, 332, 367
176, 178, 184, 194, 198, 199, 217, 220, 292, 300, Personality disorders (PD), 116, 203, 332
303, 317, 324, 341, 348, 350, 351, 357–362, 367, Pervasive anxiety, 45–51, 235
370, 372, 395, 396, 403, 405, 406, 412, 457 Pharmacology, 360–362
Medications, 57–59, 64, 65, 85, 142, 143, 145, 148–151, Phobias, 7–22, 32, 45–52, 55–56, 58–61, 75, 102, 106,
164, 261, 262, 275, 294, 296, 309, 340, 341, 347, 115, 116, 126, 129, 130, 142, 145, 157, 173, 176,
348, 351–353, 360, 361, 417 177, 179, 181–185, 205, 206, 211, 222, 235–245,
Medicine, 349, 353 249, 253–256, 259, 261, 262, 272, 273, 276, 299,
Mental health, 21, 81, 98, 113, 125–127, 130–132, 142, 301, 302, 305–307, 347–350, 357, 358, 379, 381,
164, 204, 218, 259, 261, 278, 279, 282, 321, 323, 382, 384, 432, 433, 449–453, 455, 457
347, 359, 368, 419, 425, 426, 428, 430, 434–438, Posttraumatic stress disorder (PTSD), 8, 29–39, 49, 50,
451, 455, 457, 458 100, 221, 261, 304, 315–324, 357, 359, 360, 415,
Models, 4, 5, 10, 11, 22, 32, 45–51, 57, 59, 61, 62, 64, 416, 453, 454
75–77, 81, 85, 97, 99–103, 105–107, 111–118, Progress monitoring, 131, 435
120, 125–133, 147, 148, 150, 158–160, 163, 173, Psychiatry, 3, 113, 173, 180, 261, 347, 417
175–178, 181, 182, 185, 186, 194, 196, 198, Psychology, 3, 105, 111, 125, 191, 227, 431
203–209, 211, 212, 217, 219, 220, 222, 226, 227, Psychopathology, 3, 5, 9, 32, 33, 35, 36, 39, 105, 106,
236, 240, 242, 250, 253, 273, 274, 291, 293, 295, 111, 112, 127, 128, 160, 162–165, 173, 174, 179,
300, 302, 303, 305, 307, 315–319, 322, 324, 331, 191, 194, 203–212, 259, 279, 304–305, 323, 324,
337, 372–374, 386, 399, 401, 411, 412, 414, 416, 332–335, 383, 395, 418, 420, 445, 447, 450
419, 426, 428, 429, 432, 435, 437, 438, 447 Psychopharmacology, 6, 150, 294, 349, 352, 353, 456
Mutism, 287–296 Psychotherapy, 164, 317–320, 322, 347, 411, 419
N R
Neurochemistry, 55, 56, 58, 60, 66 Recurrent thoughts, 30, 33, 34, 39, 73, 331
Neuropsychology, 38 Reliability, 3, 5, 21–22, 30, 37, 38, 82, 107, 113, 125,
Neuroscience, 145, 195, 197 179, 180, 197, 203, 208, 252–257, 272, 273,
Neurotransmission, 55, 56, 60, 77, 81, 82, 85 335–337, 381–384, 400
O S
Obsessive-compulsive disorder (OCD), 4, 8, 12, 13, School-based intervention, 307, 321, 426
29–39, 47, 48, 50, 55, 56, 64–66, 73–86, Schools, 4, 13, 16–18, 20, 30, 31, 33, 35–37, 100, 118,
103–105, 115, 126, 142, 173, 181–184, 235, 237, 130, 132, 146, 150, 151, 164, 182, 183, 250, 251,
251, 254, 256, 259, 261, 304, 331–341, 347, 349, 255, 257, 262, 271, 273, 274, 280–282, 287–290,
352, 379–381, 383, 384, 395, 397–406, 415, 416, 292, 293, 299, 301–304, 307, 309, 317, 320–322,
448, 450, 453, 455, 456 333, 336, 373, 384, 385, 397, 405, 413, 425–438,
445–448, 450–453, 456, 457
Secondary depression, 157–166
P Selective mutism (SM), 4, 50, 80, 287–296, 449, 450
Panic disorder (PD), 7, 14–16, 19–22, 32, 47, 48, 52, 56, Selective norepinephrine reuptake inhibitors (SNRI), 58,
57, 60–64, 75–78, 80, 82, 83, 98, 115, 116, 126, 261, 262, 308, 347, 350
129, 142, 158–160, 205, 206, 237, 250, 252, 276, Selective serotonin reuptake inhibitors (SSRI), 58, 59,
300, 332, 357, 358, 447–449, 455 65, 85, 148, 149, 261, 262, 275, 308, 309, 341,
Parenting, 98, 120, 127, 147, 148, 150, 162, 164, 191, 347, 348, 353
193, 217–227, 243, 251, 252, 300, 307, 309, Separation anxiety disorder (SAD), 7, 8, 16–22, 35, 47–50,
317, 320, 396, 400–405, 411, 413, 415, 52, 56, 59, 60, 142, 143, 145, 146, 157, 164, 198,
417–419, 427 208, 223, 237, 239, 249–262, 271–273, 275, 300,
Parents, 5, 12, 17, 18, 20–22, 29, 36, 37, 49, 74, 84, 100, 347, 349, 350, 352, 384, 416, 433, 446, 447
117–120, 129, 131, 143, 145, 147, 148, 150, 157, Social anxiety disorder (SAD), 8, 12–14, 20–22, 30,
163, 164, 178, 194, 217–227, 235, 238, 241, 242, 35, 37, 47, 56, 74, 75, 82, 115, 119, 120, 157,
250–262, 272, 274–280, 291, 295, 296, 299–301, 219, 221–223, 251, 259–262, 271, 272, 299,
303, 304, 306, 307, 309, 317, 319, 320, 322, 323, 300, 308, 309, 349, 350, 379, 381, 397, 431,
333–340, 352, 368, 371, 372, 374, 381–385, 433, 448–450
472 Index
Social disability, 445–458 348–353, 358, 360, 369, 370, 379–386, 389,
Social justice, 438 396–402, 404–406, 411, 412, 414–419, 428,
Specific, 3–13, 15, 17–22, 29, 30, 32, 34, 35, 38, 39, 430, 433, 434, 437, 438, 446–457
45–51, 56, 60, 61, 75, 77–80, 82, 84, 98, 100, 103,
106, 111, 113, 114, 116–118, 125–129, 131, 141,
142, 146–151, 157, 158, 160, 161, 166, 173, 174, T
178, 180, 181, 185, 186, 191, 195–197, 205–207, Taxometrics, 97–107, 112
209, 211, 217, 218, 220–223, 225, 235–245, 256, Taxonomic, 29, 111, 112
259, 271, 272, 274, 279, 280, 288, 296, 303, 304, Teachers, 37, 117, 119, 146, 147, 150, 195, 196, 279,
315, 316, 318, 320, 323, 324, 332, 334, 337, 339, 289, 290, 292, 293, 295, 299, 301, 304, 307,
347, 357, 358, 361, 369, 371, 372, 374, 379, 382, 426–431, 433–435, 438, 449, 454, 456
384, 387, 395–397, 400, 402–405, 413, 415, Transdiagnostic, 33, 84, 97, 125–133, 158, 165, 191,
417–419, 431–433, 445, 449–452, 454–458 198, 199, 217, 437, 438
Specific anxiety disorders, 6, 45, 77, 78, 118, 191, 207, Treatments, 3–6, 8, 10, 13, 15, 18, 19, 21, 22, 29, 30,
220, 221, 455, 456 36, 38, 39, 45, 47, 49–51, 55, 58–66, 73, 76,
Specific phobia (SpPh), 7–13, 17–22, 32, 56, 60, 61, 75, 83–85, 97, 99, 101, 102, 104, 106, 112–114,
106, 142, 145, 146, 173, 206, 208, 235–245, 256, 118–120, 125–133, 141–143, 145–151, 158,
272, 357, 358, 379, 384, 433, 449–452, 455 164–166, 173, 175, 182, 184, 198, 207, 220,
Substance use, 13, 15, 38, 97, 98, 126, 205, 209, 250, 221, 224–227, 236–245, 252, 253, 255–257,
300, 319, 320, 323, 357–362 259–262, 271–282, 287–296, 301–309, 315–324,
Symptom clusters, 100, 111, 116 332, 333, 335–341, 347–353, 357–362, 368–375,
Symptoms, 8, 12–22, 29–39, 47, 49, 57–59, 61–63, 65, 380–389, 395–406, 411–415, 417–420, 425, 426,
74, 75, 78–80, 82–84, 86, 97–100, 102–106, 428–435, 437, 447, 450, 454–456, 458
111–114, 116–120, 125–128, 130–133,
141–144, 146–150, 158–166, 183, 184,
192–194, 198, 204–208, 210, 211, 217–226, V
236, 238, 249–253, 255, 258–262, 272–275, Validity, 3, 22, 30, 37, 38, 98, 112, 117, 118, 128, 159,
277–279, 287–289, 293–295, 299–301, 165, 179, 180, 197, 211, 252–257, 259, 272, 273,
305–308, 315, 316, 318–324, 331–338, 340, 291, 302, 335–337, 381–384, 400, 417

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Dean McKay

Eric A. Storch Editors

ISBN 978-3-031-14079-2 ISBN 978-3-031-14080-8 (eBook)

22 Obsessive-Compulsive Disorder in Children

25 Food Neophobia in Children: Misnomer, Anxious Arousal,

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 3

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 7

Role of Avoidance Differential Diagnosis

 istinguishing Between Different

Nicole Fleischer, Jonathan Rabner,

Introduction order also met criteria for an additional disorder

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 29

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 45

Table 4.2 Content specificity in anxiety disorders

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 55

Serotonin Mechanistically, serotonin (5-HT) is

Generalized Anxiety Disorder inconsistent, with some studies demonstrating

date, no systematic investigation of serotonin Specific Phobia

Conclusion American Psychiatric Association. (2013). Diagnostic

disorder: A review. JAMA Psychiatry, 75(10), Gorman, J. M. (2000). Neuroanatomical hypoth-

study. Psychiatry and Clinical Neurosciences, 73(7), of-­concept. Neuropsychopharmacology, 38(12),

Paul D. Arnold, Lilit Antonyan, Francis Routledge,

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 73

other neurodevelopmental disorders) (Gazzellone family-based and case-control samples). In case-­

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 97

 axometric Findings for Children

t­ axonicity, and the researchers were able to repli- Anxiety Disorders

Table 7.1 Taxometric findings for anxiety disorders by sample age

Fear Fear is a key characteristic of anxiety dis-

is that fear conditioned by an aversive stimulus Conclusion and Future Directions

The diagnosis of anxiety disorders in children  SM-5-TR Diagnostic Categories

Alternate Conceptualizations was negatively correlated with both depression

p­ redisposition with environmental/psychological anxiety disorder without attention to the identi-

Laboratory-observed behavioral disinhibition in the negative affect self-statement questionnaire among

Ashley R. Karlovich , Elizabeth R. Halliday ,

FRIENDS, a universal, school-based preventa- American Psychiatric Association. (1980). Diagnostic

Alasdair Vance, Jo Winther, and Elham Shoorcheh

 DHD and the Clinical Presentation

­ edications for ADHD such as clonidine, imip-

Robert W. Garvey, Michelle K. Hiner, Chris A. Kelly,

A high rate of comorbidity between anxiety and  omorbidity Among Specific

maturation related to the psychophysiology of  isk Factors for Comorbid

wide range of anxiety states (Taylor, 1999). References

Kristel Thomassin, Marni L. Jacob, Kara B. West,

 heoretical Foundations of Emotion

Environmental Foundations able and potentially dangerous (Becker &

 motion Regulation Considerations

Introduction Personality disorders in the DSM-5 are

development of internalizing psychopathology instead demonstrating comorbidity with Cluster

Review of Literature and cope are increased, which facilitates devel-

l­ongitudinal experimental designs (McLeod on fathers’ overcontrolling behaviors, with mixed

(Crawford & Manassis, 2001). Taken together,  he Role of Parenting in Specific

Challenging Parenting Behavior intentional teasing. Results indicated that moth-

Introduction (e.g., dogs or bees) while later gains in abstract

T. E. DavisIII (*) · J. Guidry

Comorbidity also appears to be the rule for Epidemiology

Etiology studies specifically focused on youth and aspects

gresses by initially developing the graduated fear Modeling and Participant

Treatment Components and exposure to the stimulus (Davis et al., 2009b,

Table 16.1 Hypothetical example of the progression of Table 16.1 (continued)

implemented. If, following implementation, only References

Symptom Presentation activities (e.g., sleepovers, play dates). To meet

Assessment and Diagnosis Cultural context Culture may influence symp-

3-week and 3-month intervals (March et al., 1997)

22 Obsessive-Compulsive Disorder in Children

25 Food Neophobia in Children: Misnomer, Anxious Arousal,

Role of Avoidance Differential Diagnosis

istinguishing Between Different

Introduction order also met criteria for an additional disorder

Generalized Anxiety Disorder inconsistent, with some studies demonstrating

date, no systematic investigation of serotonin Specific Phobia

Conclusion American Psychiatric Association. (2013). Diagnostic

study. Psychiatry and Clinical Neurosciences, 73(7), of-concept. Neuropsychopharmacology, 38(12),

other neurodevelopmental disorders) (Gazzellone family-based and case-control samples). In case-

axometric Findings for Children

t axonicity, and the researchers were able to repli- Anxiety Disorders

is that fear conditioned by an aversive stimulus Conclusion and Future Directions

The diagnosis of anxiety disorders in children SM-5-TR Diagnostic Categories

Alternate Conceptualizations was negatively correlated with both depression

p redisposition with environmental/psychological anxiety disorder without attention to the identi-

DHD and the Clinical Presentation

edications for ADHD such as clonidine, imip-

A high rate of comorbidity between anxiety and omorbidity Among Specific

maturation related to the psychophysiology of isk Factors for Comorbid

heoretical Foundations of Emotion

Environmental Foundations able and potentially dangerous (Becker &

motion Regulation Considerations

Introduction Personality disorders in the DSM-5 are

Review of Literature and cope are increased, which facilitates devel-

longitudinal experimental designs (McLeod on fathers’ overcontrolling behaviors, with mixed

(Crawford & Manassis, 2001). Taken together, he Role of Parenting in Specific

Challenging Parenting Behavior intentional teasing. Results indicated that moth-

Introduction (e.g., dogs or bees) while later gains in abstract

Comorbidity also appears to be the rule for Epidemiology

Etiology studies specifically focused on youth and aspects

gresses by initially developing the graduated fear Modeling and Participant

Symptom Presentation activities (e.g., sleepovers, play dates). To meet

Assessment and Diagnosis Cultural context Culture may influence symp-

Introduction tion, etiology, and treatment practice with other

Other Considerations (Elizur & Perednik, 2003; Bradley & Sloman,

ocial Phobia and Anxiety Inventory

Pharmacological Treatment ment on self-report and parent-report measures.

Background form in an attempt to alleviate distress or prevent

Family Factors washing behaviors together with a child, or other

indicated in parent-child conflict. Parent psycho- Clinician-Administered Measures

(FAS-IR) is a clinician-administered, semi- Cognitive Beliefs

Cognitive-Behavioral Therapy that parents understand that accommodating mal-

Delivery Options for CBT Pharmacotherapy

Introduction term. It is important to recognize that most SSRI

Benzodiazepines to establish efficacy or safety of buspirone for the

Tricyclic Antidepressants (TCAs) Selecting medications for treatment of child and

afety, Adverse Effects,

reatment Approach #2: In Vivo

Clinical Interviews symptoms of ASD and symptoms of other diag-

Verbal, visual, and physical prompts can also Behavioral Strategies

strive to project confidence in the techniques and Treatment Studies

School-Based Intervention Program Description

Outcome Studies with 42% and 37% of students classified as

mately amplify the effect of the disorder across Panic Disorder

COVID-19 and Sociocontextual pate, understand, and address potential

easures. It is essential that development be an